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Collecting tubules from each lobe of the kidney (pyramid and its covering of cortex) discharge urine into the calyceal system via renal papillae at the entrance of each pyramid into the calyx proper antibiotic resistance process generic ampicillin 500 mg fast delivery. These collecting tubules originate deep within the radial striations (medullary rays) of the kidney and convey urine formed in the structural units of the kidneys how long on antibiotics for sinus infection to feel better ampicillin 500 mg purchase with amex, the nephrons virus that shuts down computer cheap ampicillin 250 mg on line. The parenchyma of each kidney contains approximately 1 × 10 tightly packed nephrons antibiotics for ear infections discount ampicillin online mastercard, each one consisting of a tuft6 of capillaries (the glomerulus) invaginated into the blind treatment for uti home remedies purchase ampicillin australia, expanded end (glomerular corpuscle) of a long tubule that leaves the renal corpuscle to form the proximal convoluted tubule in the cortex. This leads into the straight tubule, which loops down into the medullary pyramid (loop of Henle) and hence back to the cortex to become continuous with the distal convoluted tubule. This then opens into a collecting duct that is common to a number of nephrons and passes through the pyramid to enter the lesser calyx at the papilla. It is in these parts of the nephron (proximal tubule, loop of Henle, distal tubule, and collecting duct) that urine is formed, concentrated, and conveyed to the ureters. The distal convoluted tubule comes into very close contact with the afferent glomerular arteriole, and the modified cells of each form the juxtaglomerular apparatus, a complex physiologic feedback control mechanism contributing in part to the precise control of intra- and extrarenal hemodynamics that is a hallmark feature of the normally functioning kidney. As is the case for the renal tubules, the vasculature of the kidney is highly organized. The renal artery enters the kidney at the hilum and then divides many times before producing the arcuate arteries that run along the boundary between cortex and outer medulla. Interlobular arteries branch from arcuate arteries toward the outer kidney surface, giving rise as they pass through the cortex to numerous afferent arterioles, each leading to a single glomerular capillary tuft. The barrier where filtration from the vascular to tubular space within the glomerulus occurs is highly specialized and includes fenestrated negatively charged capillary endothelial cells and tubular epithelial cells (podocytes) separated by a basement membrane. Normally, selective permeability permits approximately 25% of the plasma elements to pass into the Bowman capsule; only cells and proteins more than 60 to 70 kDa cannot cross. However, abnormalities of this barrier can occur with disease, which 3509 may permit filtration of much larger proteins and even red blood cells; these changes manifest as the nephrotic syndrome (proteinuria >3. The glomerular capillaries exit Bowman capsule and merge to form the efferent arteriole and peritubular capillaries that nourish the tubules. The renal vasculature is unusual in having this arrangement of two capillary beds joined in series by arterioles. Blood supply to the entire tubular system comes from the glomerular efferent arteriole, which branches into an extensive capillary network. Some of these peritubular capillaries, the vasa recta, descend deep into the medulla to parallel the loops of Henle. The vasa recta then return in a cortical direction with the loops, join other peritubular capillaries, and empty into the cortical veins. Figure 50-1 A: The gross anatomy and internal structure of the genitourinary system and kidney. B: Internal organization of the kidney includes cortex and medulla regions and the vasculature. D: Plasma filtration occurs in the glomerulus; 20% of plasma that enters the glomerulus passes through the specialized capillary wall into the Bowman capsule and enters the tubule to 3510 be processed and generate urine. The functions of the kidney are many and varied, including waste filtration, endocrine and exocrine activities, immune and metabolic functions, and maintenance of physiologic homeostasis. As well as tight regulation of extracellular solutes such as sodium, potassium, hydrogen, bicarbonate, and glucose, the kidney also generates ammonia and glucose and eliminates nitrogenous and other metabolic wastes including urea, creatinine, bilirubin, and other uremic toxins (i. Finally, circulating hormones secreted by the kidney influence red blood cell generation, calcium homeostasis, and systemic blood pressure. The kidney fulfills its dual roles of toxin excretion and body fluid management by filtering large amounts of fluid and solutes from the blood and secreting waste products into the tubular fluid. Effects on the normal filtration and reabsorption processes of comorbid disease, surgery, and anesthesia are the focus of the next section. Glomerular Filtration Production of urine begins with water and solute filtration from plasma flowing into the glomerulus via the afferent arteriole. The ultrafiltration constant (Kf) is directly related to glomerular capillary permeability and glomerular surface area. Recent general revisions of Starling’s original 3511 formula to incorporate the newly appreciated importance of the endothelial glycocalyx layer also appear to be relevant to glomerular filtration, particularly for pathologic states that involve proteinuria (e. Renal autoregulation of blood flow and filtration is accomplished primarily by local feedback signals that modulate glomerular arteriolar tone to protect the glomeruli from excessive perfusion pressure (Fig. Several mechanisms for regulating blood flow to the glomerulus have been described, and all involve modulation of afferent glomerular arteriolar tone. The myogenic reflex theory holds that an increase in arterial pressure causes the afferent arteriolar wall to stretch and then constrict (by reflex); likewise, a decrease in arterial pressure causes reflex afferent arteriolar dilatation. Chloride also acts as the feedback signal for control of efferent arteriolar tone. In response to angiotensin, efferent arteriolar constriction increases glomerular pressure, which increases glomerular filtration. It is important to realize that autoregulation of urine flow does not occur, and that above a mean arterial pressure of 50 mmHg there is a linear relationship between mean arterial pressure and urine output. Tubular Reabsorption of Sodium and Water Active, energy-dependent reabsorption of sodium begins almost immediately as the glomerular filtrate enters the proximal tubule. Here, an adenosine triphosphatase pump drives the sodium into tubular cells while chloride ions passively follow. Glucose, amino acid, and other organic compound reabsorption are strongly coupled to sodium in the proximal tubule. Notably, no active sodium transport occurs in the loop of Henle until the medullary thick ascending limb is reached. Cells of the medullary thick ascending limb are metabolically active in their role of reabsorbing sodium and chloride and have a high oxygen consumption compared with the thin portions of the descending and ascending limbs. Reabsorption of water is a passive, osmotically driven process tied to the reabsorption of sodium and other solutes. Water reabsorption also depends on peritubular capillary pressure; high capillary pressure opposes water reabsorption and tends to increase urine output. The proximal tubule reabsorbs approximately 65% of filtered water in an isosmotic fashion with sodium and chloride. The descending limb of the loop of Henle allows water to follow osmotic gradients into the renal interstitium. However, the thin ascending limb and medullary thick ascending limb are relatively impermeable to water and play a key role in the production of concentrated urine. Only 15% of filtered water is reabsorbed by the loop of Henle; the remaining filtrate volume flows into the distal tubule. Conservation of water and excretion of excess solute by the kidneys would be impossible without the ability to produce concentrated urine. The arterial baroreceptors are activated when hypovolemia leads to a decrease in blood pressure, whereas atrial receptors are stimulated by a decline in atrial filling pressure. The Renin–Angiotensin–Aldosterone System Renin release by the afferent arteriole may be triggered by hypotension, decreased tubular chloride concentration, or sympathetic stimulation. Aldosterone stimulates the distal tubule and collecting duct to reabsorb sodium (and water), resulting in intravascular volume expansion. Sympathetic nervous system stimulation may also directly cause release of aldosterone. Stress states, renal ischemia, and hypotension stimulate the production of renal prostaglandins through the 3514 enzymes phospholipase A and cyclooxygenase. Clinical Assessment of the Kidney Most agree that immediate perioperative measures such as urine output correlate poorly with perioperative renal function ; however, much about the4 kidneys can be learned from knowing how effectively they clear circulating substances and inspection of the urine (i. Renal Function Tests Filtration is a useful method to clinically assess kidney function. As a key indicator of disease, knowledge of limited filtration capacity is important to guide drug dosing for agents cleared by the kidneys and helps with preoperative risk stratification. Also, acute declines in filtration capacity indicate kidney injury and predict a more complicated clinical course. However, despite creatinine’s limitations, its relatively steady supply from muscle metabolism, modest tubular secretion, and proven usefulness in numerous clinical settings make it the most used renal filtration marker currently available. In stable, critically ill patients, 2- hour urine collections are sufficient to calculate CrCl, using the following11 formula: where U = urine creatinine, V = total volume of urine collected, P =cr cr plasma creatinine, and time = collection time. Nonetheless, serum creatinine remains, so far, an unsurpassed perioperative tool, particularly to reflect trends of change in renal filtration and to predict outcome, even during the perioperative period. Urinalysis and Urine Characteristics Urine inspection can reveal abnormal cloudiness or color and unexpected odors. Detailed descriptions or of urine examination are available ;22 therefore, only a summary is provided here. Cloudy urine is due to suspended elements such as white or red blood cells and/or crystals. Lightly centrifuged urine sediment will normally contain 80 ± 20 mg of protein per day and up to two red blood cells per high-power field (400×); higher levels of red blood cells or protein reflect abnormal kidney function. Urine protein electrophoresis can differentiate proteinuria from a glomerular (filtering), tubular (reuptake), overflow (supply that saturates the reuptake system), or tissue (e. In contrast, color changes reflect dissolved substances; this occurs most commonly with dehydration, but other causes include food colorings, drugs, and liver disease (e. Chromogenic dipstick chemical tests can determine urine pH and provide a semiquantitative analysis of protein, blood, nitrites, leukocyte esterase, glucose, ketones, urobilinogen, and bilirubin. In addition, microscopy can identify crystals, cells, tubular casts, and bacteria. Urine specific gravity (the weight of urine relative to distilled water) normally ranges between 1. The normal response to4 hypovolemia is renal solute retention; fluid and electrolyte retention produces a concentrated urine with a low sodium content (<20 mEq/L). Perioperative Nephrology Pathophysiology Altered renal function can be thought of as a clinical continuum ranging from the normal compensatory changes seen during stress to frank renal failure. Clinically, there is considerable overlap between compensated and decompensated renal dysfunctional states. The kidney under stress reacts in a predictable manner to help restore intravascular volume and maintain blood pressure. The net result of modest activity of the stress response system is a shift of blood flow from the renal cortex to the medulla, avid sodium and water reabsorption, and decreased urine output. Electrolyte Disorders Disorders of Sodium Balance Hyponatremia is the most commonly occurring electrolyte disorder (see also Chapter 16). Intravascular volume status and urinary sodium concentration are key markers in differentiating the large number of potential causes of hyponatremia. If water excess is a reason for hyponatremia, a dilute urine with a sodium concentration above 20 mmol/L is expected. Conversely, avid renal sodium retention (urine sodium <20 mmol/L) suggests sodium loss as a cause. If hyponatremia is acute, the risk of 3519 neurologic complications is higher, and cautious treatment is indicated to prevent cerebral edema and seizures. This should be accomplished with intravenous hypertonic saline and furosemide to enhance water excretion and prevent sodium overload (see transurethral resection syndrome section). Hypernatremia (serum sodium >145 mmol/L) is generally the result of sodium gain or water loss, most commonly the latter. Dehydration of brain tissue can cause symptoms ranging from confusion to convulsions and coma. In cases of hypernatremia, laboratory studies often show evidence of hemoconcentration (increased hematocrit and serum protein concentrations). Occasionally, the urine is not maximally concentrated, suggesting an osmotic diuresis or an intrinsic renal disorder such as diabetes insipidus. The primary goal of treatment is restoration of serum tonicity, which can be achieved with isotonic or hypotonic parenteral fluids and/or diuretics unless irreversible renal injury is present, in which situation dialysis may be necessary. Disorders of Potassium Balance Even minor variations in serum potassium concentration can lead to symptoms such as skeletal muscle weakness, gastrointestinal ileus, myocardial depression, malignant ventricular dysrhythmias, and asystole. Circulating potassium levels are tightly controlled via renal and gastrointestinal excretion and reabsorption, but potassium also moves between the intra- and extracellular compartments under the influence of insulin and β -adrenoceptors. In the kidney, 70% of2 potassium reabsorption occurs in the proximal tubule and another 15% to 20% in the loop of Henle. The collecting duct is responsible for potassium excretion under the influence of aldosterone. Hypokalemia may be due to a net potassium deficiency or transfer of extracellular potassium to the intracellular space. Notably, total body depletion may exist even with normal extracellular potassium levels (e. Hypokalemia treatment involves supplementation by either intravenous or oral route; however, extreme caution should be used with intravenous potassium administration because 3520 overly rapid delivery can cause hyperkalemic cardiac arrest. Disorders of Calcium, Magnesium, and Phosphorus Most of a grown adult’s 1 to 2 kg of calcium is in bone (98%), with the remaining 2% in one of the three forms: ionized, chelated, or protein bound. The clinical manifestations of hypocalcemia include cramping, digital numbness, laryngospasm, carpopedal spasm, bronchospasm, seizures, and respiratory arrest. A positive Chvostek sign (facial muscle twitching in response to tapping the facial nerve) or Trousseau sign (carpal spasm induced by brachial artery occlusion) are the classic hallmarks of hypocalcemia but in practice are often absent. Mental status changes, including irritability, depression, and impaired cognition may also occur. Acute hypocalcemia due to citrate toxicity can develop from rapid infusion of citrate-stored packed red blood cells, particularly with citrate accumulation during the anhepatic phase of liver transplant procedures. Hypocalcemia due to 3521 reduced serum protein levels is physiologically unimportant. Clinical symptoms of hypercalcemia correlate with its acuity and include constipation, nausea and vomiting, drowsiness, lethargy, weakness, stupor, and coma. The most frequent causes of hypercalcemia are primary hyperparathyroidism and malignancy. Magnesium is a multifunctional cation that is found primarily in the intracellular space.

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Peripheral nerve blocks of the trigeminal nerve and occipital nerve branches may be used to provide analgesia while avoiding general anesthesia antibiotic resistant klebsiella purchase generic ampicillin online. The use of intraoperative epidural anesthesia followed by postoperative epidural local anesthetics or opioids has been popular in older children and adults antibiotic gel for acne order ampicillin on line, and these techniques are being applied to neonates antibiotic powder for wounds ampicillin 500 mg generic. In addition antibiotics for severe acne order cheapest ampicillin, most neonatologists are experienced with the intravenous administration of opioids for patient comfort antibiotics for sinus infection when allergic to penicillin cheap ampicillin american express. Commonly used systemic treatments for postoperative pain are listed in Table 42-7. Oral Routes Oral routes of medications have been used for decades in neonates and children for managing pain. The commonly used oral analgesics include 2983 nonsteroidal analgesics including acetaminophen (10 to 15 mg/kg) and ibuprofen (5 to 10 mg/kg), and opioids, including hydrocodone (0. There may be some pharmacogenetic changes associated with the use of codeine in infants; thus, it is falling out of favor in use across all ages. A larger dose than is usually given orally is needed in infants to achieve good blood levels, because of unreliable absorption. A dose of 20 to 30 mg/kg of rectal acetaminophen is generally recommended for postoperative pain control. Diclofenac, a commonly available rectal suppository in Europe, is frequently used in infants for postoperative pain control. Intravenous Analgesia Opioids are the mainstay of analgesia in neonates and infants in the postoperative period. Morphine and fentanyl are frequently used in the neonatal intensive care unit for analgesia. However, the potential for opioid tolerance after prolonged infusion of opioids is somewhat common. To decrease the likelihood of opioid tolerance, one can rotate opioids or add44 other medications including continuous intravenous naloxone142 and intravenous methadone. Other intravenous nonsteroidal anti-inflammatory medications and intravenous acetaminophen, have been introduced. Intravenous ketorolac, a nonsteroidal anti-inflammatory drug, has been used successfully 2984 in neonates and infants for pain control at a dose of 0. If the surgical procedure or the neonate’s condition is such that postoperative ventilation is likely, the prolonged respiratory effects of opioids or any other drug are of little concern. However, if the surgical procedure is relatively short and by itself does not require postoperative ventilation, the clinician should carefully select drugs, as well as doses of anesthetic drugs and relaxants, that will not necessitate prolonged postoperative ventilation or intubation. Postoperative ventilation places the neonate at added risk because of the problems associated with mechanical ventilation, the trauma to the subglottic area, and the potential development of postoperative subglottic stenosis or edema. However, if there is any question about the neonate’s ability to maintain protective airway reflexes or normal ventilation after anesthesia, the neonate should be returned to the recovery room or neonatal intensive care unit with the trachea intubated, with controlled mechanical ventilation. Special Considerations Maternal Drug Use during Pregnancy Many drugs taken during pregnancy can affect the fetus and neonate. During pregnancy, maternal drug use of cocaine, marijuana, and others leads to a host of problems for the neonate. Cocaine use, for instance, results in a reduced catecholamine reuptake, which may result in the accumulation of catecholamines. This accumulation has circulatory effects on the uterus, the umbilical blood vessels, and the fetal cardiovascular system. Three major problems affecting the infant are premature birth, intrauterine growth retardation, and cardiovascular abnormalities, including low cardiac output. The clinical implication of this finding is that these neonates may be unstable enough in the first day of life that it may be advantageous to postpone surgery, if possible, until the second or third day of life. There is also an increase in structural cardiovascular malformations and electrocardiographic abnormalities. Temperature Control and Thermogenesis The newborn is at risk for significant metabolic derangements caused by hypothermia. Newborns, and especially preterms, do not have the normal compensatory mechanisms that infants and children have when exposed to a cold environment. The newborn does not shiver, increase activity, or effectively vasoconstrict like older children or adults do in response to cold. In addition, the newborn has a larger body surface area-to-weight ratio that promotes heat loss, as well as low levels of subcutaneous fat for insulation. The primary mechanism the newborn has to respond to heat loss is nonshivering thermogenesis. Norepinephrine stimulates increased metabolism in a specialized tissue, brown fat, which contains a high concentration of mitochondria and has abundant vascular supply. Stimulated lipolysis results in heat production, with side effects of increased oxygen consumption and production of ketone bodies and water. The aerobic activity results in diversion of cardiac output to the deposits of brown fat around the kidneys, under the sternum, and between the scapulae. Because the diuresis, diversion of cardiac output away from the core circulation, and metabolic acidosis are maladaptive, every effort should be made to prevent nonshivering thermogenesis in the newborn. Efforts to minimize nonshivering thermogenesis in the newborn are based on minimizing heat loss, both during transport to and from the neonatal intensive care unit and in the operating room. Transport should be done with the newborn in an incubator or in an open bed with overhead heaters. In the operating room, the room temperature is raised to its maximal level to minimize loss by conduction. Placing the patient on a forced-air warming blanket can reduce conductive heat loss. Using plastic wrap or commercially available covers and hats to minimize heat loss from the head and all other areas not in the surgical field is also beneficial. The goal of all these activities is to maintain a neutral thermal environment, minimizing the stress that hypothermia can induce in the perioperative period. A complicating factor is that anesthetic agents can reduce or eliminate thermogenesis, removing any ability to compensate for cold stress. Characteristics include airway smooth muscle hyperplasia, peribronchiolar fibrosis, enlarged alveoli, and disorganized pulmonary vasculature. Many patients improve as they age, but reactive airways, recurrent pulmonary infections, and a prolonged oxygen requirement are seen in some patients. Anesthetic concerns in these patients include evaluation of baseline oxygenation and potential presence of active bronchoconstriction. These patients often benefit from prophylactic bronchodilator therapy before induction. The baseline measure of oxygenation is important because these patients have less pulmonary oxygen reserve and may desaturate quickly with induction of anesthesia and hypoventilation. Although postanesthetic ventilation is not usually required, a high index of suspicion should be used if there is significant clinical evidence of poor lung function preoperatively. Postoperative Apnea Apnea and bradycardia are well-recognized, major complications during and after surgery in neonates. The infants at highest risk are those born prematurely, those with multiple congenital anomalies, those with a history of apnea and bradycardia, and those with chronic lung disease. Decreased ventilatory control and decreased responsiveness to hypoxia and hypercarbia may be potentiated by anesthetic agents. Respiratory muscle fatigue may also play a role because neonates have a smaller percentage of type I fibers in their diaphragm and intercostal muscles. In addition, hypothermia and anemia also contribute to the development of postoperative apnea. However, some infants require mask ventilation or even prolonged intubation and ventilatory 2987 support. Caffeine and theophylline (metabolized to caffeine) act by increasing central respiratory drive and lowering the threshold of response to hypercarbia, as well as stimulating contractility in the diaphragm. Caffeine is favored because of its wider therapeutic margin and decreased propensity for toxicity. Administering caffeine prophylactically to infants at risk of postoperative apnea to ensure adequate serum levels may prevent the need for prolonged periods of postoperative ventilatory support. The question remains as to which infant should be admitted and monitored after outpatient surgery and for how long. The most conservative approach is to monitor all infants younger than 60 weeks’ postconceptual age overnight after surgery. Although the incidence of significant apnea and bradycardia is highest in the first 4 to 6 hours after surgery, it can occur up to 12 hours after surgery. An insightful approach to interpreting the various small studies is to stratify the risk of apnea, as done by Cote et al. Using 95% confidence limits, the authors found that the probability of apnea in nonanemic infants free of recovery room apnea was not less than 5% until postconceptual age was 48 weeks with gestational age of 35 weeks. This risk was not less than 1%, until a postconceptual age of 56 weeks with a gestational age of 32 weeks or a postconceptual age of 54 weeks and gestational age of 35 weeks. This type of analysis allows the clinician to determine which patients should be admitted on not only the criteria of gestational and postconceptual ages but also the amount of risk they are willing to assume. The very preterm infant, especially those under 1,200 g of weight, are at highest risk, with an incidence of significant disease about 2%. Acute retinal changes are seen in about 45% of susceptible preterm neonates, but there is spontaneous regression in most, permitting development of normal vision. In the fetus, developing blood vessels grow gradually 2988 from the macula toward the edges of the developing retina. In full-term newborns, this process is complete at birth or in the first few weeks, but continues for a longer period in the preterm infant. These growing vessels are at risk for vasoconstriction and subsequent hemorrhage, followed by disorganized neovascularization or scarring. This scarring and lack of normal growth can eventually cause the retinal network to peel away resulting in retinal detachment. Many children who develop stage I improve with no treatment and eventually develop normal vision. The abnormal blood vessels grow toward the center of the eye instead of following their normal growth pattern along the surface of the retina. Plus disease means that the blood vessels of the retina have become enlarged and twisted, indicating a worsening of the disease. The most common therapies involve using cryotherapy or laser therapy to destroy peripheral areas of the retina, slowing or reversing the abnormal growth of blood vessels. This is done to preserve the central vision from continuing distortion of the abnormal vessels in the periphery, although there is some loss of peripheral vision with this therapy. Cryotherapy and laser therapies, as well as advanced procedures, are usually performed under general anesthesia in the operating room, although it is occasionally done at bedside with sedation in ventilated patients. These surgical procedures do not involve blood loss or significant surgical stress, but they do depend on a still surgical field for periods ranging from 30 to 90 minutes. The primary anesthetic challenge in these patients is related to the 2989 extreme prematurity and small size of the patients. Adequate monitoring, vascular access, and thermal stability are common challenges to management. There is no direct answer to this question, but some evidence from a large collaborative study helps provide some guidance. This study demonstrates that the use of supplemental oxygen for a prolonged period of time, not just for the short duration of a general anesthetic, was not deleterious as long as the pulse oximetry readings were kept in the 96% to 99% range. Neurodevelopmental Effects of Anesthetic Agents There has been recent concern about the potential deleterious impact of anesthetic drugs on the developing brain. A variety of studies have shown that prolonged exposure of animal models to anesthetic agents can lead to neurodegenerative changes in the developing brain of neonatal rats. The collective data that are currently available in literature do not support the withdrawal of these drugs from the practice of neonatal anesthesia. The neurotoxicity data seem to be reproducible in rodents but not in other species. Future prospective trials with prospective neurocognitive testing of infants exposed to anesthesia are needed. There currently exists no conclusive evidence to demonstrate the deleterious effect of inhaled or intravenous 2990 anesthetics on neurocognitive function in neonates and infants. Prospective studies, including a current study randomizing infants to getting a spinal anesthesia versus general anesthesia should be able to provide better information on this very complex problem that may face pediatric anesthesiologists. There has been a strong trend in recent years to put an emphasis of presurgical stabilization before taking the newborn to the operating room. Exceptions to this include gastroschisis, which is usually corrected within 12 to 24 hours, airway lesions such as webs that are causing significant airway obstruction, and acute subdural/epidural hematomas from traumatic delivery. In most cases, however, a period of 1 to 3 days can be allowed for stabilization of the newborn or transport to an appropriate pediatric center for treatment. There is more to neonatal emergency surgery than just the immediate anesthetic and surgical procedures. Many of these infants require the support services of specialized nursing units, pediatric radiologists, pediatric intensive care physicians, specialized laboratory facilities, and they must have their complete care be the main consideration of where their surgery should be done. Many procedures are now performed using laparoscopic techniques which decreases postoperative morbidity and pain and facilitates early extubation. Because of the lack of expertise many hospitals have in the care of these patients, the transfer of these neonates to hospitals with greater expertise is often prudent after initial stabilization of the patient. Most hospitals that have expertise in these patients have a transport team that is well-qualified to help with stabilization and transport. Those centers that do not have transport teams often have extensive protocols and procedures to work with the sending institution to help ensure the safe transfer of the patient. Two confounding factors in neonatal surgery are prematurity and associated congenital anomalies.

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Although he calculated that etomidate dose should not require adjustment for shock antibiotic resistance over prescribing order ampicillin online now, the authors decrease the dose by at least 25% to 50% when hypovolemia is suspected antibiotic shelf life discount ampicillin 250 mg buy. As to the opioids bacteria 3 domains buy generic ampicillin line, the calculated dose for fentanyl and remifentanil is approximately one-half that for healthy patients (Fig treatment for uti bactrim buy 250 mg ampicillin overnight delivery. Figure 53-11 Calculated dose reduction of various anesthetics administered as bolus or infusion in moderate hemorrhagic shock virus nyc purchase ampicillin online. Calculation is based on pharmacokinetic and pharmacodynamic studies performed in experimental hemorrhagic shock. For example, the baroreceptor depression produced by intravenous agents is usually milder than that of 3809 inhalational agents. Opioid agents have little direct cardiovascular or baroreflex depressant effect; however, these agents can cause hypotension by inhibiting central sympathetic activity, especially in the hypovolemic trauma patient whose apparent hemodynamic stability is maintained by hyperactive sympathetic tone. Two important principles in the use of anesthetic agents are accurate estimation of the degree of hypovolemia and reduction of doses accordingly. The presence of hypotension suggests uncompensated hypovolemia, in which case anesthetics almost invariably produce further deterioration of systemic blood pressure and sometimes cardiac standstill. When time constraints or continuing hemorrhage prevent restoration of blood volume, the airway may be secured without the benefit of anesthesia (perhaps using only rapidly acting muscle relaxants and small doses of opioids, etomidate, or ketamine), even though this approach may result in recall of induction and intraoperative events in up to 40% of patients, and, as mentioned before, vital organ ischemia. Intraoperative use of the bispectral index monitor and, whenever possible, titrating anesthetics to bispectral index levels lower than 60 may prevent recall in trauma patients. In normotensive but hypovolemic patients, restoration of volume and selection of an agent with the least cardiovascular depressant effect appears logical. Ketamine and etomidate are the preferred induction agents,257 although at low doses other intravenous anesthetics are also unlikely to produce hypotension. Therefore, the use of any of these drugs in reduced doses is probably more important than the particular agent chosen. Maintenance of anesthesia in the hypovolemic trauma patient raises concerns similar to those pertaining to induction. Under these circumstances, patients are unlikely to respond to the sympathetic effect of N O, and the cardiovascular2 depressant properties of the gas are unmasked. In addition, by reducing FiO , use of N O incurs a2 2 risk of hypoxemia in patients with reduced cardiac output or pulmonary compromise. Despite causing little impairment of reflex tachycardia and having a vasodilatory activity that preserves organ blood flow in normovolemic patients, isoflurane can impair cardiac output and organ blood flow in hypovolemia—that is, it can cause cardiovascular depression. Desflurane and sevoflurane are not significantly better than isoflurane in this regard. However, because of their low solubility in blood, the severe hemodynamic depression produced by these agents can be rapidly reversed, preventing suboptimal perfusion for a significant period of time. Head and Open Eye Injuries The importance of deep anesthesia and adequate muscle relaxation during airway management of patients with head or open eye injuries has already been discussed. Hypotension caused by anesthetics or other factors contributes to the development or progression of cerebral ischemia. This problem can be ameliorated by administering pretreatment doses of opioids (fentanyl, 2 to 3 μg/kg), which permit reduction of the anesthetic dose. Nevertheless, myoclonus is best prevented by careful timing of the dose of muscle relaxants. Isoflurane has the least vasodilatory effect and thus is the most widely used inhalation anesthetic, although desflurane and sevoflurane have comparable effects on the cerebral circulation. In these patients, anesthesia can be maintained initially with opioids plus propofol, midazolam, or etomidate. Although there are unavoidable shortcomings to the study, it nevertheless indicates that the specific anesthetic agents chosen probably do not affect the neurologic outcome as long as the vital signs are maintained. Cardiac Injury If there is pericardial tamponade, preload and myocardial contractility must be maintained. A decrease in heart rate should also be treated promptly to maintain adequate cardiac output. Because 3812 all of the available anesthetics can depress myocardial contractility and cause vasodilation, it is preferable to administer these agents after evacuation of the pericardial blood under local anesthesia. If general anesthesia is required to relieve the tamponade, induction should be delayed until the patient is prepared and draped. Deep anesthesia and high airway pressures should be avoided before evacuation of the hemopericardium. In chronic pericardial effusion, ketamine supports the cardiac index better than other intravenous agents. In acute pericardial tamponade, even minor insults can bring cardiac activity to a halt. Similar principles apply to the use of maintenance agents, which should be given in the smallest possible doses until the heart is decompressed. In blunt myocardial injury, the objective is not only to maintain cardiac contractility but also to lower the elevated pulmonary vascular resistance that may result from concomitant pulmonary contusion, atelectasis, or aspiration. All anesthetics should preferably be administered after restoration of intravascular volume and titrated to maintain adequate systemic blood pressure and cardiac output. If necessary, inotropes, preferably amrinone or milrinone, which produce some pulmonary vasodilation, may be used. Anesthetic maintenance by intravenous anesthetics and opioids to avoid the myocardial depression produced by inhalational agents should also be considered. Burns A hypermetabolic state characterized by tachycardia, tachypnea, catecholamine surge, increased O consumption, and augmented catabolism2 follows the initial few hours of a burn and continues into the convalescent phase, necessitating increased oxygen, ventilation, and nutrition. Usually, an autograft harvested from either the patient, a cadaver, or both is used. Needle electrodes or surgical staples, a reflectance pulse oximeter, and an arterial catheter may be necessary. The administration of a large amount of blood and blood products subjects the patient to complications of transfusion, such as hypocalcemia and coagulopathy, requiring monitoring of coagulation status and administration of adequate replacement therapy. During the hyperdynamic phase, blood flow to the liver and kidneys increases with increasing cardiac output. Thus drugs that rely on organ blood flow for elimination are cleared at a faster rate, requiring larger doses for effect, which may also be associated with hemodynamic depression. Morphine may be the preferred opiate; in a preliminary study, patients receiving fentanyl experienced higher body temperatures than those who received morphine. This was attributed to the well-established anti- inflammatory properties of morphine. Increased opioid requirement is related not only to the intense pain level but also to tolerance, which starts developing about 3 to 4 weeks after injury, reaching a maximum at 10 to 17 weeks and gradually declining to baseline about 6 months after injury. For serial wound debridement, dressing or line changes, and insertion of urinary catheters in children, ketamine in intermittent doses provides a suitable alternative to inhalation anesthesia. Hemodynamic stability, preserved airway patency, bronchodilation, anti-inflammatory effect, counteraction of opioid hyperalgesia, and maintenance of hypoxic and hypercapnic responses are all advantages of this agent. Dysphoria and increased salivary output can be overcome by concomitant administration of benzodiazepines and anticholinergics. It should be kept in mind that in some catecholamine-depleted burn patients, hypotension may follow ketamine administration. Regional anesthesia in its various forms can be effective to provide intraoperative anesthesia, postoperative analgesia, and assistance for rehabilitation. Pain in these patients originates from the burn site but also the area of skin harvesting, and often the latter is more intense. Tumescent infiltration in the form of continuous infusion of local anesthetic administered subcutaneously at the donor site may provide satisfactory analgesia. Lateral cutaneous nerve or transverse abdominis plane blocks provide analgesia to the lateral thigh, where skin harvesting is usually performed. These blocks may be combined with fascia iliaca blocks if the graft is taken from the anterior thigh. Paravertebral blocks with or without catheter placement can provide excellent analgesia to burnt areas at the torso. Brachial plexus and sciatic/femoral blocks can be useful for upper and lower extremity pain management. Finally, if the patient’s back is free of burn injury, neuraxial blocks can be used. The mechanism of this response is related to upregulation (increase) of acetylcholine receptors, which ultimately occupy the entire muscle membrane, and the additional expression of two newly described isoforms of the acetylcholine receptor, and nicotinic (neural) α -acetylcholine7 receptors. The latter can be depolarized not only by acetylcholine and succinylcholine but also by choline, which thus plays an important role in the development of hyperkalemia. For instance, rocuronium, which is important for rapid-sequence induction and treatment of laryngospasm when succinylcholine is contraindicated, has an onset time delayed by about 50 seconds (30% longer than patients without burn) when a 0. Recovery time from the block is shorter in burned patients than in normal individuals. Although many other causes, such as citrate intoxication (hypocalcemia), hypothermia, coronary artery disease, allergic reactions, or incompatible transfusion may be responsible for this complication, they occur infrequently. The source may be obvious, such as external bleeding from the skull or an open vessel in the extremities, or occult. The thoracic and abdominal cavities and the pelvic retroperitoneal space are the most common sites of occult hemorrhage that results in hypotension. Management includes early diagnosis and control of the bleeding site plus effective fluid resuscitation with a rapid-infusion system, which should be connected to a 14-gauge or larger cannula, preferably inserted into veins both above and below the diaphragm. Neurogenic shock from spinal cord injury may be missed during initial evaluation, especially in unconscious patients. Patients with spinal cord injury are often bradycardic and readily respond to catecholamine administration. Mistaking neurogenic shock for hemorrhagic shock may lead to excessive fluid infusion and pulmonary edema in the spinal cord–injured patient. The reverse error may also occur, depriving patients with hemorrhagic shock of fluids because of misdiagnosis of neurogenic shock. Equalization of pressures across the cardiac chambers during diastole suggests pericardial tamponade. This effect, however, is rare and is usually associated with critical hemodynamic instability. Differential diagnosis in these instances can be established by pericardiocentesis. Decreasing the rate of fluid infusion in these patients results in a further decrease in cardiac output. Treatment includes fluid infusion, pulmonary vasodilators if the systemic blood pressure is normal, and inotropic support if the systemic blood pressure is low. Absence of response to this treatment is an indication for placement of an intra-aortic balloon pump. Pulmonary artery catheterization may also help detect an oxygen step-up from a septal injury. Hypothermia 3817 Shock, alcohol intoxication, exposure to cold, fluid resuscitation, and abnormalities in thermoregulatory mechanisms render the major trauma patient hypothermic during the initial phase of injury. A core body temperature below 35°C is often associated with acidosis, hypotension, and coagulopathy, which in turn may lead to an increased risk of severe bleeding, need for transfusion, and mortality. Admission hypothermia, which is89 present in approximately 50% of patients, is an independent risk factor after major trauma,272 and the mortality rate increases with decreasing temperature. Severe hypothermia, which in the trauma patient is defined as core temperature below 32°C,273 was associated with a 100% mortality rate in one study,274 although survival of a few patients with admission temperatures even lower than 32°C has been reported. Increased heat loss is seen most commonly in patients with spinal cord, extensive soft tissue, and burn injuries and in patients who consumed ethanol preoperatively or those undergoing body cavity surgery. Other deleterious effects of hypothermia are cardiac depression, myocardial ischemia, arrhythmias, peripheral vasoconstriction, impaired tissue oxygen delivery, elevated oxygen consumption during rewarming, blunted response to catecholamines, increased blood viscosity, metabolic acidosis, abnormalities of K and Ca+ 2+ homeostasis, reduced drug clearance, and increased risk of infection. For each liter of fluid given at 40°C to a patient with a body temperature of 33°C, 29. In severe trauma, thrombin binds to thrombomodulin, which slows or reduces the activation of thrombin-activated fibrinolysis inhibitor, leading to hyperfibrinolysis. It interferes with the generation of thrombin, a factor essential in activating cofactors, platelets, and enzymes, in addition to converting fibrinogen to fibrin. However, the differential diagnosis between consumptive and dilutional coagulopathy requires laboratory testing. At lower Hct level, clot may develop but may not be strong enough to overcome bleeding. Component transfusion therapy, used universally in civilian trauma, is inferior to the whole blood transfusion practiced by the military. During storage, red cells undergo changes, including the loss of adenosine triphosphate, diphosphoglycerate, and potassium; oxidative injury to proteins, lipids, and carbohydrates; loss of shape and membrane; increased adhesiveness; decreased flexibility; reduced flow in capillaries; and decreased oxygen delivery. The success of a blood transfusion is defined as 75% of the red cells infused still being effective after 24 hours. The storage injury brings out the controversy about the safety and effectiveness of “new blood” versus “old blood. Although banked blood can be stored for 42 days, the average age of blood units used in busy trauma centers is 16 days, essentially slightly older than “new blood. The significant complication of these additives is that citrate chelates calcium, which serves as a co-factor in the coagulation cascade, leading to hypocalcaemia. In addition to defective coagulation, signs and symptoms of hypocalcemia include hypotension, decreased pulse pressure, arrhythmias, change in mental status, and tetany. After centrifuging and removing the supernatant, the remaining precipitate contains high concentrations of procoagulant factors in a small volume of plasma. Fibrinogen levels are commonly low upon arrival to the trauma emergency room and are effectively replaced with cryoprecipitate during the early phase of trauma management. On the other hand, tranexamic acid 3823 given beyond 3 hours of injury increased bleeding-related mortality. Antifibrinolytics, especially tranexamic acid, should be considered in patients who demonstrate fibrinolysis during serial thromboelastographic or thromboelastometric monitoring. Currently most trauma centers are using tranexamic acid routinely during the initial resuscitation with continuation into the intraoperative phase. Thus to obtain any benefit, it should be administered after platelet and fibrinogen levels are adequate and pH and hypothermia are corrected to at least 7.

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In this image from a normal kidney antibiotic vs anti infective cheap ampicillin 500 mg overnight delivery, there are two medullary rays with three rows of nephrons aligned per- pendicular to the medullary ray tubules Fig antibiotics and yogurt discount ampicillin 250 mg online. Notice that there are no medullary rays and that there is no evidence of nephron atrophy or metanephric dysgenesis Fig 2 virus 68 in children purchase 250 mg ampicillin. Although the normal kidney should have 10–14 generations of nephrons antibiotics pink eye 500 mg ampicillin purchase overnight delivery, identifying more than 9 to 10 genera- tions in a well-oriented section is difficult infection 2 game hacked order 250 mg ampicillin fast delivery. Others, like the author, agree with reflux-related injury, but believe most cases are developmental in origin as a result of in utero reflux that damages the developing renal lobe. Segmental hypoplasia is defined as a small kidney with a deep cortical groove(s) and dilatation of adjacent calyx. The cortex contains few tubules, with no or only rare glomeruli, little or no inflammation, and no evidence of metanephric dysgen- esis or nephron atrophy. The medulla is absent or flattened with no loops of Henle and may contain a distinctive cellular Fig 2. This kidney is from a 17-year-old patient interstitial mesenchymal tissue not present in the normal renal with cortical hypoplasia. Extrarenal vascular anomalies occur in 40 % of cases of three nephron generations are present, and there is no atrophy or supporting a developmental abnormality. This example of segmental hypoplasia shows the circumferential deep cortical groove characteristic of segmen- tal hypoplasia. Only two to three nephron generations are present, and there is no atrophy or metanephric dysgenesis Fig. It is only 7 cm in length and contains a single circumferential deep cortical groove and dilated collecting system. In addition to the segmental hypoplastic focus, there was cortical hypoplasia with a reduc- tion in nephron generation to two to three generations in sections of oth- erwise normal cortex away from the groove, as shown in Fig. This developmental abnormality strengthens the postulate that segmental hypoplasia may have a developmental basis, at least in some cases Fig. There are multiple hyp- glomeruli are present to indicate an atrophic lesion oplastic foci, and the renal pelvis is significantly dilated 28 2 Developmental Anomalies and Cystic Kidney Diseases Fig. It demonstrates the abrupt case shows the abrupt transition from normal cortex to the hypoplastic transition from normal cortex to the hypoplastic focus. The hypoplastic focus contains dilated veins, hypertrophied focus contains dilated veins, hypertrophied arteries, and several small arteries, infrequent small tubules, and mild inflammation. No tubular atrophy or glomerulosclerosis is atrophy, normal glomeruli, or glomerulosclerosis is present present Fig. This hypoplastic segment from the kidney of a 33-year-old woman shows how narrow the hypoplastic foci may be. Notice the normal cortex on both sides of the lesion and the characteristic abrupt transition. The hypoplastic focus contains thick- walled arteries, dilated veins, and no evidence of normal or sclerotic glomeruli 2. Potter syn- The most extreme form of reduced renal mass is renal agenesis drome results in neonatal death from pulmonary hypoplasia or complete absence of kidney and ureter. Renal agenesis because amniotic fluid is required for proper lung develop- may be unilateral or bilateral. Neonates with Potter syndrome also have extrarenal radic or part of several malformation syndromes. Bilateral anomalies known as the Potter sequence or oligohydramnios agenesis is often referred to as Potter syndrome. The Potter sequence includes Potter facies, illus- kidneys are responsible for producing much of the amniotic trated later, and varus deformity of the lower extremities. Because the ureter contributes to the formation of the trigone musculature, the trigone will be abnormal. Male patients with unilat- eral agenesis often have no mesonephric duct–dependent structures and Fig. Louis: Mosby; 2008: Although the adrenals are present, both kidneys and ureters are absent. The renal disease varies greatly in sever- bilateral renal dysplasia, and distal complete urinary tract obstruction) ity. The most severe forms affecting neonates and infants lead will have Potter facies, which includes a broad beaked nose; bilateral epicanthic folds; low-set, often posteriorly rotated ears; and a recessed to death related to pulmonary hypoplasia. The impaired pul- mandible monary development is attributed to the massively enlarged kidneys that compromise the thoracic space. This is a useful histologic finding in older patients in whom the renal findings may not be diagnostic. In surviving chil- dren, the liver abnormality is usually progressive, resulting in congenital hepatic fibrosis and death due to complications related to portal hypertension. The kidneys are reniform but diffusely cystic, with both cortex and medulla affected by cysts Fig. The thoracic space is very small because the massive kidneys impeded lung development. Thus, this infant died from respira- tory failure due to pulmonary hypoplasia Fig. The diffuse and uniform character of the cysts is apparent and imparts a spongy appearance, thus the term sponge kidney. However, it should not be confused with medullary sponge kid- ney, a completely different disorder Fig. The kidneys are congested, but numerous tiny cysts are faintly visible through the thin renal capsule 32 2 Developmental Anomalies and Cystic Kidney Diseases Fig. Because the kidney size is not dramatically increased, normal pulmonary development occurred and survival into childhood or young adulthood was possible. In this case, the kidneys are enlarged but less so than in the neonatal presentations. The nephrons, glomeruli, and proximal and distal tubules are usually normal but appear inconspicuous between the cystic collecting ducts 2. Although the cystic disease appears less severe that the interstitium is expanded with fibrosis. No interstitial fibrosis or atrophic cysts may be small and usually are rounded in profile. There also is changes have developed ectasia of other tubules, likely proximal tubules. Most cysts are located in the renal medulla, affecting concentration function 34 2 Developmental Anomalies and Cystic Kidney Diseases Fig. The bile ducts reside in an with congenital hepatic fibrosis shows marked fibrous portal expansion expanded portal triad and are peripherally arrayed and branched. This patient had liver abnormality may be a useful finding in cases in which the renal portal hypertension. Masson trichrome stain lesion is less severe and the diagnosis is more challenging. However, several other cystic kidney diseases also may have a bile duct plate mal- formation and develop congenital hepatic fi brosis Fig. Bile duct abnor- malities are present, and the portal tract is expanded as the result of dense portal fi brosis 2. They encode for the proteins polycystin 1 and well as the most common genetic kidney disease, with an 2, respectively. Essentially no normal renal parenchyma is present, making it difficult to distinguish cortex from medulla Fig. The cysts’ contents vary from clear, to opaque fluid, to hemorrhagic, and may become infected or contain calculi Fig. Whenever cysts are encountered in someone younger than 40 years, a hereditary cyst dis- Fig. This partial nephrectomy was ease should be considered performed in a child because of concern about a cystic neoplasm. The liver cyst lining is smooth and glistening because it is lined by mucinous epithelium (From Zhou M, Magi-Galluzzi C, editors. Cysts may become symptomatic if large or if secondary complications, such as infection, occur Fig. In this section, two large cysts are present, likely arising in a single nephron Fig. No large popula- tion-based studies have been performed 38 2 Developmental Anomalies and Cystic Kidney Diseases Fig. The intervening cortical tissue shows tubular atrophy, inter- stitial fi brosis, and mild chronic in fl ammation 2. The tufts and papillary formations usually are lined by a single layer of cytologically bland epithelium Fig. Histologically, there would be advanced nephro- sclerosis and tubulointerstitial scarring Fig. Notice that the epithelium is bland and single layered, with no nuclear pleomorphism or mitotic activity 40 2 Developmental Anomalies and Cystic Kidney Diseases Fig 2. In addition, the patient was known to have been on dialysis for many years and did not have cysts at the initiation of dialysis Fig. The most distinctive and unique microscopic proliferative lesions affecting renal tubules. This is an incipient neoplasm whose size is below the threshold described with this fi nding that merits a neoplastic designation. This tumor has a solid, papil- lary, or microcystic architecture and is composed of vacuolated cells with eosinophilic cytoplasm. They often localize to the medulla but which there is a localized collection of cysts that affect an commonly also involve the cortex. When only a portion of entire kidney, or a portion of a kidney, with a normal non- the kidney is involved, the lesion usually is regarded preop- cystic contralateral kidney. In this case, there is extensive cystic disease affecting most, but not all, of the kidney. The differential would be resolved by a combination of clinical and histologic fi ndings 44 2 Developmental Anomalies and Cystic Kidney Diseases 2. This most often is a sporadic event with a low likelihood of a subsequently affected fetus. Alternatively, it may be syndromic, occurring in many multiple malformation syndromes, or may be part of a nonsyndromic multiple malformation syndrome. The kidneys themselves may range from large and diffusely cystic (so-called multicystic dysplasia or cystic dysplasia) to small kidneys with few or no cysts (so-called aplastic kidney or aplastic dysplasia). The histologic severity of the metanephric dysgenesis varies widely, ranging from extensive cyst formation with few primitive nephron ele- ments, to islands of differentiating tissue that contain normal-appearing nephrons that may exhibit corticomed- ullary differentiation but are not connected to a collecting system, to extensive zones of seemingly well-developed kidney with only a modest number of cysts or dysgenetic nephrons. Between the larger cysts are normal Most examples of renal dysplasia are associated with tubules. The ureter of the affected segment may be atretic, stenotic, or massively dilated, or the urethra may be atretic or obstructed by a pos- terior urethral valve, a situation usually associated with bilat- eral disease. The lower urinary tract lesions are regarded as part of the malformation sequence rather than the culprit responsible for renal maldevelopment. The nonsyndromic dysplasias are broken down into sev- eral categories based on the anatomic distribution of renal involvement. A simple classification of nonsyndromic renal dysplasia is as follows: • Unilateral • Bilateral • Segmental dysplasia associated with duplex kidney The following images provide a sampling of the spectrum of renal dysplasia that may be encountered, beginning with sporadic and nonsyndromic multiple malformation events. It is not possible to distinguish a lining cells usually are flattened unless papillary hyperplasia is present, as illustrated in Figs. Imaging the contralateral kidney is nonsyndromic from syndromic event based on the renal required for accurate diagnosis, which is a diagnosis of exclusion fi ndings. This is an example of a 1-cm dysplastic kidney from an adult kidney is enlarged and diffusely cystic, whereas the left kidney is with vaginal ureteral ectopia. Patients with multicystic dys- Because no urine is formed in utero, oligohydramnios developed. This is a second-trimes- ter termination of pregnancy for bilateral multicystic dysplasia. Bilateral multicystic dysplasia is a lethal condition because of failure of amniotic fluid production necessary for pulmonary devel- opment. Although both lungs and the diaphragm have been removed, the small size of the thoracic cavity is evident 46 2 Developmental Anomalies and Cystic Kidney Diseases Fig. The bladder is massively distended because of the presence of posterior urethral valves Fig. Ureteral abnormalities such as atresia, stenosis, and hydroureter are commonly encountered with multicystic dysplasia. The classification of renal cystic diseases and other congenital anoma- lies of the kidney and urinary tract. This is a unique exam- ple of ureteral malformation associated with bilateral multicystic dys- plasia. This example of bilateral renal aplasia was associated with massive hydroureters secondary to urethral atresia. The kidneys are small and the adrenal glands appear large by comparison as they drape over the kidneys. Although there is urethral atresia, the bladder is not massively dilated because of a rectal-vesicle fi stula. Notice the rectum on the right 48 2 Developmental Anomalies and Cystic Kidney Diseases Fig. The renal abnormalities will not always be identical, even in the face of a common distal obstruction. It shows a large multicystic left kidney and a much smaller, albeit still dysplastic, right kidney Fig. In most cases with in utero complete urinary tract obstruction, bilateral renal dysplasia is an expected finding.

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An alternate theory antibiotic resistance understanding and responding to an emerging crisis cheap ampicillin line, the guarded- receptor theory antibiotics for acne what to expect generic ampicillin 250 mg mastercard, assumes that the intrinsic binding affinity remains essentially constant regardless of a channel’s conformation; rather treatment for dogs eating grapes purchase ampicillin 500 mg, the apparent affinity is associated with increased access to the recognition site resulting from channel gating antibiotic resistance deaths order ampicillin on line. Figure 22-5 Diagram of the bilayer lipid membrane of conductive tissue with the sodium channel spanning the membrane bacteria h pylori infection order ampicillin now. The neutral base (N) is more lipid soluble, preferentially partitions into the lipophilic membrane interior, and + easily passes through the membrane. Molecular determinants of state-dependent block of Na channels by local anesthetics. To get to its site of action, principally the voltage-gated sodium channels, local anesthetics have to reach the targeted nerve membrane. This entails the diffusion of drugs through tissues and the generation of a concentration gradient. Even with close proximity of deposition, only about 1% to 2% of injected local anesthetics ultimately penetrate into the nerve. As discussed earlier, the perineural sheath encasing24 nerve fibers appears to be an important determinant; nerves that have been desheathed in vitro require about a 100-fold lower local anesthetic concentration (in the 0. Although it may vary with anatomic location and nerve physiology, functional block typically occurs within 5 minutes of injection in rat sciatic nerves, and this time course corresponds to the peak in the intraneural drug absorption. The degree of nerve blockade depends on the local anesthetic concentration and volume. For a given drug, a minimal concentration is necessary to effect complete nerve blockade. It reflects the potency of the local anesthetics and the intrinsic conduction properties of nerve fibers, which 1441 in turn likely depend on the drug’s binding affinity to the ion channels and the degree of drug saturation necessary to halt the transmission of action potentials. Accordingly, individual types of nerve fibers differ in their minimal blocking concentration, such that some A fibers are blocked by lower drug concentrations than C fibers. A sufficient volume is needed to suppress the regeneration of nerve impulse over a critical length of nerve fiber. Transmission stops once the membrane27 depolarization falls below the threshold for action potential activation. If the exposure distance is inadequate, action potentials can “skip” over blocked segments and resume nerve conduction. In contrast, exposure over a long segment of nerve to even a relatively low drug concentration can still result in gradual extinction of impulse by decremental decay. It has long been observed that application of local anesthetics produces an ordered progression of sensory and motor deficits, starting commonly with the disappearance of temperature sensation, followed in order by proprioception, motor function, sharp pain, and finally light touch. Termed differential blockade, historically this had been thought to be related simply to the diameter of the nerve fibers, with the smaller fibers inherently more susceptible to drug blockade than larger fibers. However, although the “size28 principle” of differential blockade is consistent with many experimental findings, it is not universally true. Larger, myelinated Aδ fibers (believed to mediate sharp pain) are preferentially blocked over small, nonmyelinated C fibers (dull pain). Furthermore, within the C fibers are fast and slow components of impulse transmission, each with distinct susceptibilities to drug blockade. These observations argue against a purely pharmacokinetic29 mechanism as the sole explanation for differential blockade. The first node of Ranvier at left contains no local anesthetic and gives rise to a normal action potential (solid curve). If the nodes succeeding the first are occupied by a concentration of local anesthetic high enough to block 74% to 84% of the sodium conductance, then the action potential amplitudes decrease at successive nodes (amplitudes are indicated by interrupted bars representing three increasing concentrations of local anesthetic). Eventually, the impulse decays to below-threshold amplitude if the series of local anesthetic–containing nodes is long enough. Propagation of the impulse is then blocked by decremental conduction, even though none of the nodes are completely blocked. Concentrations of local anesthetics that block more than 84% of the sodium conductance at three successive nodes prevent any impulse propagation at all. Pharmacology and Pharmacodynamics Chemical Properties and Relationship to Activity and Potency Most clinically relevant local anesthetics consist of a lipid-soluble, aromatic benzene ring connected to an amide group via either an amide or an ester moiety. The type of linkage broadly defines them into two 1443 categories, the aminoesters and the aminoamides, and affects how they are metabolized. Aminoesters are hydrolyzed by plasma cholinesterases and aminoamides are degraded by hepatic carboxylesterases. Some metabolites of aminoesters, such as para-aminobenzoic acid, can induce immunologic reactions and are responsible for the slightly greater incidence of severe allergic reactions associated with aminoesters. Other than these characteristics, physiochemical properties of both aminoesters and aminoamides are similar and are mainly determined by their dissociative constant, lipophilic makeup, and spatial arrangement of the molecule. The tertiary amide on local anesthetics can accept a proton at low affinity; thus, these compounds are classified as weak bases. In aqueous solution, local anesthetics are in constant equilibrium between the protonated cationic form and the lipid-soluble neutral form. The ratio of the two forms depends on the pKa or the dissociation constant of the local anesthetics and the surrounding pH (Table 22-3). A ratio with high concentration of the lipid-soluble form favors intracellular entry, as the cellular membrane restricts passage of the cationic form, but not the lipid soluble form. Clinically, the proportion of the2 lipid-soluble form can be increased by alkalization of local anesthetic solution and thus accelerate the onset of action. Once inside the cell, equilibrium is reestablished between the cationic and the neutral forms, and experimental findings have shown that the cationic form is principally responsible for blockade of sodium channels. Lipid solubility of local anesthetics is conferred by the composition of alkyl substitution on the amide and the benzene groups. In the laboratory, lipid solubility is measured by the partition coefficient in a hydrophobic solvent, octanol, and compounds with high octanol:buffer partition coefficient are more lipid soluble. A positive correlation exists34 between the potency of the local anesthetics and their octanol:buffer partition coefficient; highly lipid-soluble agents are more potent and tend to have a longer duration of action than ones that are less lipid soluble. The first is at the level of cellular entry as greater lipid solubility facilitates passage through the lipid membrane barriers. Detailed crystallographic findings show that local anesthetics bind to a hydrophobic pocket within the sodium channels and suggest that ligand binding may be mediated primarily by hydrophobic and van der Waals interactions (Fig. Compared with experimental setups using isolated nerves, many other factors may influence the potency of local anesthetics on nerves in situ. Highly36 1444 lipid-soluble agents may be sequestered into surrounding adipose cells and myelin sheaths. Local anesthetics cause vasodilation, which in turn could alter regional drug redistribution. Hence,31 relative potency of local anesthetics has been determined clinically for different applications, and these values are listed in Table 22-4. Finally, anesthetic activity and potency are affected by the stereochemistry of the local anesthetic molecules. Many older drug preparations exist as racemic mixtures; that is, enantiomeric stereoisomers are in equal proportion. Newer agents, namely, ropivacaine and levobupivacaine, are available as specific enantiomers. Although the desired improvement in the safety index has been generally supported in clinical studies, this is at the expense of a slight decrease in potency overall and shorter duration of action compared with racemic mixtures. Topographic features at the channel-binding site are likely to play a key role in stereoselectivity of local anesthetics. Table 22-3 Physicochemical Properties of Clinically Used Local Anesthetics Table 22-4 Relative Potency of Local Anesthetics for Different Clinical Applications Additives to Increase Local Anesthetic Activity 1445 Epinephrine Reported benefits of epinephrine include prolongation of local anesthetic block, increased intensity of block, and decreased systemic absorption of local anesthetic. Epinephrine’s vasoconstrictive effects augment local anesthetics41 by antagonizing inherent vasodilating effects of local anesthetics, decreasing systemic absorption and intraneural clearance, and perhaps by redistributing intraneural local anesthetic. The smallest dose is suggested because epinephrine combined with local anesthetics may have toxic effects on tissue, the cardiovascular system, peripheral nerves, and45 46 the spinal cord. As previously discussed, the neutral form is believed to be important for penetration into the neural cytoplasm, whereas the charged form primarily interacts with the local anesthetic receptor within the sodium channel. Therefore, the rationale for alkalinization was to increase the ratio of local anesthetic existing as the lipid-soluble neutral form. However, clinically used local anesthetics cannot be alkalinized beyond a pH of 6. Together, alkalinization of local anesthetics appears limited as50 a clinically useful adjuvant to improving anesthesia. Opioids Opioids have multiple central and peripheral mechanisms of analgesic action (see Chapter 20). Spinal administration of opioids provides analgesia primarily by attenuating C-fiber nociception and is independent of51 supraspinal mechanisms. Coadministration of opioids with central neuraxial52 local anesthetics results in synergistic analgesia. An exception to this53 analgesic synergy is chloroprocaine, which appears to decrease the effectiveness of opioids coadministered epidurally. The reason is unclear,54 but the mechanism does not seem to involve direct antagonism of opioid receptors. Nonetheless, clinical studies support the practice of central55 neuraxial coadministration of local anesthetics and opioids for prolongation and intensification of analgesia and anesthesia. However, although some studies have reported favorable56 outcomes for such coadministration, others have failed to demonstrate any 1447 increased efficacy. A problem that has plagued many studies is the lack of57 adequate controls for differentiating the analgesic effects of opioids acting peripherally versus a more central mechanism resulting from systemically absorbed opioids. Nonetheless, recent carefully designed trials have shown that some opioids, namely, buprenorphine, may enhance and prolong postoperative analgesia better than either local anesthetics alone or local anesthetics administered with intramuscular buprenorphine. Clonidine also has direct inhibitory effects on61 peripheral nerve conduction (A and C nerve fibers). Thus, addition of62 clonidine may have multiple mechanisms of action depending on the type of application. Preliminary evidence suggests that coadministration of an α -2 agonist and local anesthetic results in central neuraxial and peripheral nerve analgesic synergy, whereas systemic (supraspinal) effects are additive. On63 64 average, clonidine improves the duration of analgesia by about 2 hours, regardless of whether an intermediate- or long-acting local anesthetic is used. Overall, results from clinical trials indicate that clonidine can enhance65 local anesthetic effects when used for intrathecal and epidural anesthesia and peripheral nerve blocks. Experiments in animals using extended-release preparations of local anesthetics have found that addition of dexamethasone to the mixture prolongs the conduction block after peripheral nerve application. Clinical reports of the use of69 dexamethasone as an adjuvant to local anesthetics have shown similar prolongation of anesthesia after brachial plexus blockades70,71 and intravenous regional anesthesia. Combined with intermediate- to long-acting72 local anesthetics, dexamethasone extends the duration of analgesia by approximately 50% after supraclavicular or interscalene approaches to the70 71 brachial plexus block (Fig. Although initial laboratory data show no evidence of increased neurotoxicity from use of dexamethasone as compared with other adjuvants, our current understanding of its mechanism of action 1448 and potential side effects remains incomplete. Currently, such preparations are approved for local infiltration of surgical wounds after bunionectomy and hemorrhoidectomy. Data are shown as the Kaplan–Meier survival density estimates, with the shaded region representing the 95% confidence interval. Effect of dexamethasone on the duration of interscalene nerve blocks with ropivacaine or bupivacaine. Clinically, most frequently reported untoward effects of liposomal79 bupivacaine were nausea and pyrexia. Having a thorough understanding of the factors involved would enable one to maximize the local anesthetic potential while avoiding possible complications arising from systemic local anesthetic toxicity. Systemic Absorption Decreasing systemic absorption of local anesthetics increases their safety margin in clinical uses. The rate and extent of systemic absorption depends on the site of injection, the dose, the drug’s intrinsic pharmacokinetic properties, and the addition of a vasoactive agent. The vascularity of the tissue markedly influences the rate of drug absorption, such that deposition of local anesthetics in vessel-rich tissues results in higher peak plasma levels in a shorter period of time. Accordingly, the rate of systemic absorption is greatest with intercostal nerve blocks, followed in decreasing order by caudal and epidural injections, brachial plexus block, and femoral and sciatic nerve blocks (Table 22-6). Thus, the same amount of local anesthetics injected would result in unequal peak plasma levels depending on the site of drug delivery. For a given site of injection, the rate of systemic absorption and the peak plasma level are directly proportional to the dose of local anesthetic deposited. In general, more potent lipid-soluble agents are associated with a slower rate of absorption than less lipid-soluble compounds (Fig. Local anesthetics exert direct effects on vascular smooth muscles in a concentration-dependent manner. At low concentrations, more potent agents appear to cause more vasoconstriction than less potent agents, thereby decreasing the rate of vascular absorption. At high concentrations, vasodilatory effects seem to38 predominate for most local anesthetics. The pattern of distribution is largely dependent on organ perfusion, the partition coefficient between compartments, and plasma protein binding. Organs that are well perfused,82 such as the heart and the brain, have higher drug concentrations. Unfortunately, they are also the organs most seriously affected by local anesthetic toxicity. Aminoesters are hydrolyzed by plasma cholinesterases and aminoamides are transformed by hepatic carboxylesterases and cytochrome P450 enzymes. Severe liver disease may slow the clearance of aminoamide local anesthetics and significant drug levels may therefore accumulate. Bupivacaine is a more lipid-soluble and more potent agent with less systemic absorption over time. Nonetheless, pharmacokinetics are difficult to predict in any given circumstance because both physical and pathophysiologic characteristics will affect the individual pharmacokinetics. There is some evidence for increased systemic plasma levels of local anesthetics in the very young and in the elderly owing to decreased clearance and increased absorption ; however, the correlation of systemic blood levels between the84 dose of local anesthetic and weight is often inconsistent (Fig. Effects85 of gender on clinical pharmacokinetics of local anesthetics have not been well defined, although pregnancy may decrease clearance.

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Karmok, 43 years: The panel may also contain series of antibiotic that are present in specified con- centrations in the wells of applicable MicroScan panels.

Iomar, 37 years: Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.

Benito, 41 years: Atelectasis in children undergoing either propofol infusion or positive pressure ventilation anesthesia for magnetic resonance imaging.

Rathgar, 46 years: The pterygopalatine fossa is highly vascular, so care must be exercised to avoid intravascular injection.

Olivier, 24 years: Thiopental also92 has negative inotropic effects, directly by altering intracellular calcium homeostasis and indirectly by diminishing sympathetic tone.

Temmy, 25 years: Protein and fat can be metabolized 2–4 days after an operation (at the earli- est).

Lee, 44 years: It is in this tissue can be injected air at the technical errors that arise when a tracheostomy is performed.

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