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Nonprotein calories should be divided roughly equally between carbohydrates and fats for optimal growth and body composition symptoms diarrhea generic primaquine 7.5mg free shipping. The growing premature infant requires enteral intake of 5-7 g/kg/day of fat and 10-14 g/kg/day of carbohydrate treatment 5th metatarsal stress fracture primaquine 7.5mg on line. Preterm infants are able to readily absorb the saturated fats in human milk due to the composition of human milk fat and the presence of bile salt-activated lipases in human milk medicine discount primaquine 7.5mg with visa. Preterm infant formulas contain a mixture of medium chain triglycerides and polyunsaturated long-chain triglycerides that are well absorbed by premature infants treatment 1st metatarsal fracture generic 7.5 mg primaquine with mastercard. Carbohydrate is provided in the form of lactose in human milk and as a mixture of glucose polymers and lactose in premature infant formulas symptoms nausea generic 7.5mg primaquine visa. At birth medicine abuse buy primaquine 7.5mg without prescription, premature infants are deficient in intestinal lactase activity compared with full term infants, but lactase activity appears to increase at an accelerated rate following delivery, such that lactose intolerance is not an issue in premature infants. As discussed above, preterm infants quickly enter a state of negative nitrogen balance unless exogenous protein is provided, and these infants should be given a standard solution containing dextrose and amino acids beginning on the first day of life. Initially, extremely preterm infants may not tolerate glucose infusion rates of more than 5-6 mg/kg/min, but glucose tolerance typically improves over the first several days of life, and the glucose infusion rate can usually be gradually advanced to 10-11 mcg/kg/min, corresponding to about 125 ml/kg/day of a 13% dextrose solution. Amino acid infusions are well tolerated at all gestational ages and can be started at 3 g/kg/day even on the first day of life. After urine output is well established, electrolytes are added to the parenteral nutrition solution. Typical requirements include a sodium intake of 3-4 mEq/kg/day and potassium intake of 2-3 mEq/kg/day, both given as a combination of chloride and acetate salts. Calcium and phosphorus are also given, with typical calcium requirements ranging between 60-80 mg/kg/day of elemental calcium. Parenteral lipids are usually started at 1-2 days of life at an initial dose of 0. Lipid tolerance should be periodically assessed by checking triglyceride levels, which should be kept below 200 mg/dl. Approaches to the initiation and advancement of feedings Intestinal immaturity and concomitant illness are challenges to the provision of enteral feedings to extremely premature infants. In the 1970s, prolonged delays in the initiation of enteral feedings were common, largely due to concerns that feeding might contribute to the development of necrotizing enterocolitis. Since that time, a number of studies have demonstrated that "trophic" feeds, started in the first few days of life, are well tolerated and do not increase the risk of necrotizing enterocolitis. Trophic feeds have been shown to decrease the incidence of cholestatic jaundice, improve subsequent feeding tolerance, and result in better weight gain. Approaches vary, but trophic feeds are typically started at a volume of 5-20 ml/kg/day and continued at that volume for 3-5 days before the volume is advanced. Very low birth weight infants, or those with gestational age < 29 weeks, are generally appropriate candidates for trophic feedings; more mature infants do not require this approach. A coordinated suck and swallow mechanism is not present before 32 to 34 weeks of gestation, and preterm infants therefore require feeding via a nasogastric or orogastric tube. Feedings can be given as a continuous infusion or as a bolus, generally every 2 to 3 hours. The available evidence does not prove the superiority of either method, but bolus feeding is generally thought to be more physiologic, and there is some evidence that bolus feeds are better tolerated and result in better weight gain. Feedings should be full-strength human milk or preterm infant formula; there is no role for the provision of diluted milk or formula when initiating feedings. If preterm formula is used, most practitioners begin with the 24 cal/oz preparation, inasmuch as the osmolality is virtually identical to that of 20 cal/oz formula and the nutrient content is higher. Most infants achieve adequate weight gain with a caloric intake of about 120 cal/kg/day, corresponding to a feeding volume of 150 ml/kg/day of 24 cal/oz formula or fortified breast milk. Most practitioners feel that advancing feeding volume too rapidly increases the risk of necrotizing enterocolitis, but the evidence on this issue is not conclusive. Similiarly, there is not a well defined optimal rate of advancement, but most practitioners do not advance feeds more quickly than 20-30 ml/kg/day. Breast milk and breast milk fortification Breast milk contains a variety of immunoprotective factors, hormones and enzymes and is well tolerated by premature infants. It is the feeding of choice for premature infants, but preterm breast milk does not contain sufficient amounts of protein, calcium, phosphorus and certain trace elements and vitamins to optimally support growth of the preterm infant. For that reason, breast milk requires fortification with a commercially available fortifier that provides additional protein, minerals and vitamins. The nominal caloric content of breast milk is 20 cal/oz, and standard fortification with a human milk fortifier increases caloric content to 24 cal/oz. However, caloric content of breast milk may vary substantially between individuals and is partially dependent on maternal diet. In addition, milk expressed toward the end of a pumping session (hind milk) contains more fat and hence has a higher caloric content. These factors may need to be considered in an infant who is not growing well on breast milk feedings despite what initially appears to be an adequate caloric intake. Such infants may require further fortification of breast milk to achieve a caloric content that permits adequate growth. Formulas As mentioned above, preterm infant formulas contain additional protein, calcium, phosphorus and certain other minerals and vitamins to support optimal growth. Carbohydrate is provided as a mixture of lactose and glucose polymers and a portion of the fat content is provided as medium-chain triglycerides for ease of absorption. These formulas are provided as prepackaged sterile liquids and are available in a variety of caloric densities. Following discharge, premature infants may continue to need additional protein and minerals beyond what is contained in term infant formula to achieve optimal growth. These formulas have nutrient densities that are intermediate between those of preterm and term infant formula. Transitional formulas are typically used for premature infants who are approaching discharge or who weigh about 2 kg. Formula manufacturers recommend that these formulas be continued for at least 6 months following discharge, but the available data suggest that the benefits of these formulas are limited. Metabolic responses to early and high protein supplementation in a randomized trial evaluating the prevention of hyperkalemia in extremely low birth weight infants. Nutrient-enriched formula versus standard term formula for preterm infants following hospital discharge. Nutritional practices and growth velocity in the first month of life in extremely premature infants. Early provision of parenteral amino acids in extremely low birth weight infants: relation to growth and neurodevelopmental outcome. The systemic inflammatory response that is triggered by the disease can result in multiorgan failure and injury to the developing brain. In fulminant cases, affected infants may go from appearing essentially well to being critically ill in a matter of hours. Lethargy, apnea and temperature instability are common, as are abdominal tenderness and distention, absent bowel sounds, and bloody stools. Feeding intolerance is fairly common among preterm infants and is therefore not a specific indicator of disease, and it is difficult to objectively define. If the infant is essentially wellappearing, has no abdominal tenderness and minimal distention, further evaluation may not be needed. On the other hand, if the infant appears ill, has abdominal tenderness or has significant distention, then an abdominal X-ray is warranted. Pneumatosis intestinalis is manifested by linear streaks or bubbles of gas seen within the bowel wall and is thought to result from metabolic activity of bacteria that have invaded the intestinal tissue. Portal venous gas presumably represents dissection of pneumatosis intestinalis into the portal venous system. Blood gases often demonstrate significant metabolic acidosis, particularly if the disease is severe. Broad-spectrum antibiotics are given empirically and are directed against bowel flora that might seed the bloodstream across injured gut mucosa. With severe disease, multiorgan failure may develop, and the infant may require ventilatory support and blood pressure support with pressors. Serial abdominal X-rays are usually obtained early in the course of the disease, when there is risk of intestinal perforation. The time at which findings of pneumatosis intestinalis and portal venous gas resolve after diagnosis is variable and is not helpful in determining prognosis or directing ongoing therapy. In uncomplicated cases, gradual clinical improvement is usually seen after the first few days. Infants are usually kept npo and maintained on hyperalimentation for 10 days to allow for intestinal mucosal healing. In addition, it is often difficult to determine the ultimate viability of bowel that appears compromised at the time of surgery but is not frankly necrotic. In extremely low birthweight infants with perforation, placement of a peritoneal drain has been shown to result in short-term outcomes that are comparable to those achieved with open laparotomy, although between 25% and 75% of infants initially treated with a peritoneal drain will go on to require laparotomy. Relative indications for surgery include worsening peritonitis, the presence of a fixed dilated loop of bowel on X-ray, and general failure to respond to supportive care and medical management. In infants who have severe and extensive disease, laparotomy may confirm the absence of any viable bowel, leading to a decision to discontinue support. Intestinal barrier function and host defenses are impaired at various levels in the preterm gut. The premature intestinal mucosa is also relatively permeable to bacterial toxins and even intact bacteria. A variety of basic laboratory studies have shown that the immature intestine has an excessive inflammatory response to microbial stimulation. In full term infants, this inflammatory response is moderated by downregulation of different components of the epithelial innate immune response. Current evidence suggests that this developmental regulation does not occur in premature infants, predisposing them to bowel inflammation when intraluminal bacterial colonization occurs. These abnormal colonization patterns may result from prior antibiotic use as well as failure to establish initial colonization with beneficial commensal bacteria such as lactobacillus. As this inflammatory response progresses, downstream mediators trigger local vasoconstriction, leading to secondary hypoxic-ischemic injury. Intestinal mucosal integrity is thus further compromised, allowing additional bacterial invasion of intestinal tissue and further amplification of the inflammatory response. By the time the disease is diagnosed clinically, bowel inflammation is already well advanced and cannot be reversed by any currently available therapeutic intervention. These strategies have included limiting enteral feeds; breast milk feedings; both prenatal and postnatal steroid treatment; and probiotic administration. In the 1970s, this observation led to the practice of delaying the introduction of enteral feeds for prolonged periods of time and advancing feedings very slowly once they were begun. This practice clearly has many adverse nutritional consequences and has since fallen out of favor. These trophic feedings are usually continued for a period of 3-5 days before the feeding volume is advanced. Breast milk contains a variety of immunologic factors that may bolster intestinal host defenses, promote colonization with beneficial commensal bacteria, and limit intestinal inflammation. The use of donor breast milk to feed those infants whose mothers are not supplying milk has been endorsed by the American Academy of Pediatrics, but use of donor milk poses significant issues of cost and logistics that may limit its widespread use. Prenatal steroids are regularly given to accelerate lung maturity when preterm delivery is anticipated. However, early postnatal steroid treatment has been associated with worse neurodevelopmental outcomes, and postnatal steroids are not commonly used at present. Probiotics are a group of bacterial organisms, including Lactobacillus and Bifidobacteria species, that are found in large quantities in the intestinal tract of healthy individuals and are thought to play an important role in modulating intestinal inflammation and in promoting colonization with diverse bacterial species. However, these trials used various probiotic preparations, enrolled infants were not stratified according to breast milk use, and the effect was not entirely consistent across trials. Myth: necrotizing enterocolitis: probiotics will end the disease, and surgical intervention improves the outcome. Updated meta-analysis of probiotics for preventing necrotizing enterocolitis in preterm neonates. Laparotomy versus peritoneal drainage for necrotizing enterocolitis and perforation. Both anatomic and physiologic immaturities of the cerebral vasculature are mainly responsible for the unique types of hemorrhagic and ischemic cerebral injury that can occur in preterm infants. Cerebrovascular autoregulation in preterm infants Adults are able to autoregulate cerebrovascular tone over a wide range of perfusion pressures in order to maintain constant cerebral blood flow despite fluctuations in systemic blood pressure. The autoregulatory range becomes progressively lower and narrower with decreasing age, and in preterm infants, the lower limit of the autoregulatory range is thought to be close to the normal mean arterial blood pressure. When perfusion pressures are outside the autoregulatory range, the cerebral circulation becomes pressure-passive. The extent to which the cerebral circulation is pressure-passive in preterm infants is debated, but there is general agreement that pressure passivity of the cerebral circulation is a real phenomenon in preterm infants. In the pressure-passive circulation, systemic hypotension may result in cerebral hypoperfusion and ischemia, and systemic hypertension may result in excessive regional cerebral blood flow, potentially resulting in hemorrhagic injury. There is experimental evidence that marked hypocapnea can limit cerebral oxygen delivery. Conversely, hypercapnea during the first few days of life has been associated with a higher risk of germinal matrix hemorrhage. Development of the cerebral vasculature the blood supply to the brain parenchyma develops through ingrowth of arteries from the pial surface of the brain. Long penetrating arteries supply the deep periventricular white matter, and short penetrating arteries supply the more superficial areas of white matter. Development of these penetrating arteries is not complete in preterm infants, and connections between vessels are sparse.
Mixed hearing loss is when a conductive hearing loss occurs in combination with a sensorineural hearing loss professional english medicine discount 7.5 mg primaquine. Usually this occurs with large or toxic doses but it may also occur with lower doses medications ending in zole buy primaquine 15mg free shipping. Hearing loss is measured as a difference from the normal ability to detect sound relative to established standards treatment diabetic neuropathy proven primaquine 15mg. Treatment Audiologic rehabilitation assessment is provided to evaluate the impact of a hearing loss on communication functioning (strengths and weaknesses) medicine you take at first sign of cold effective primaquine 15mg, including the identification of speechlanguage-communication impairments schedule 6 medications discount primaquine 7.5 mg mastercard. Audiologic rehabilitation provides intervention to address the impairments treatment bursitis buy generic primaquine 7.5 mg on-line, activity limitations, participation restrictions, and possible Speech-Language Pathology Medical Review Guidelines 42 environmental and personal factors that may affect the communication, functional health, and well-being of persons with hearing impairment. Treatment involves compensating for the hearing loss as much as possible, and may include the fitting of a hearing aid, or the recommendation of a cochlear implant. Hearing Aids: Sound amplification with a hearing aid helps people who have either conductive or sensorineural hearing loss. Cochlear Implants: Most profoundly deaf people who cannot hear sounds even with a hearing aid benefit from a cochlear implant. Cochlear implants provide electrical signals directly into the auditory nerve by means of multiple electrodes inserted into the cochlea, which is the inner ear structure containing the auditory nerve. An external microphone and processor pick up sound signals and convert them to electrical impulses. The impulses are transmitted electromagnetically by an external coil through the skin to an internal coil, which connects to the electrodes. For infants, early detection of hearing loss and intervention services reduces the consequences of the loss. When hearing loss occurs at birth or within the first few months of life ("prelingual" onset), the impact on communication development is usually significant because the loss occurs during the time considered critical for language development. Even mild hearing loss can delay speech and language development in a young child. The audiologist selects, fits, and evaluates all forms of amplification devices for infants, children, and adults. Both speech-language pathologists and audiologists are qualified to provide audiological rehabilitation services to individuals with hearing loss. Cochlear implant users must learn a new way of processing sound and maximizing the effectiveness of the device; they benefit from intensive audiologic rehabilitation services. A language disorder is characterized by deficiencies in comprehension (understanding) and/or production (use) of spoken and written language. The impairment may involve the form of language (phonology, morphology, syntax), the content of language (semantics), or the function of language in communication (pragmatics or social communication). Treatment Intervention services are conducted for children and adults with spoken and/or written language disorders, including problems in areas of language form (phonology and alphabetic Speech-Language Pathology Medical Review Guidelines 43 symbols, morphology and orthographic patterns, and syntax), content (semantics), and/or use (pragmatics or social communication) across spoken and written modalities. Knowledge and use of language for listening, speaking, reading, writing, and thinking may include work on print symbols, syntax, and semantics, for example. Understanding and formulating complex spoken and written sentences may be a goal of treatment, as well as developing self-regulatory strategies for handling complex language and literacy demands. Laryngectomy Laryngectomy, a surgical removal of all or part of the larynx, is usually indicated to treat cancer of the larynx or vocal cords and adjacent tissues. The speech-language pathologist is also primarily responsible for evaluating and training the patient to use a tracheostomal valve for hands-free speech. Laryngectomy Related Instrumentation Speech-language pathologists use instrumentation in assessment and treatment procedures related to laryngectomy (including prosthetics) that include, but are not limited to: Electrolarynx Prosthetics An electrolarynx is a handheld device held against the throat region (or mouth with an oral adapter immediately post-op) to provide vibrations that allow speech sound. Electrolarynx Speech-Language Pathology Medical Review Guidelines 44 training is generally required. Prosthetics - Intervention services are conducted to assist individuals to understand, use, adjust, and restore their customized prosthetic/adaptive device. Tracheostomy speaking valves such as the Passy-Muir valve are considered voice prosthetics that enable the wearer to produce speech. When speech and voice disturbances do occur, they usually present as a spasticataxic dysarthria with disorders of voice intensity, voice quality, articulation, and intonation. The goal of therapy is to enhance ease and clarity of communication and promote safe swallowing and overall health. Myofunctional Disorder (Tongue Thrust; See also Myofunctional Treatment) Myofunctional disorder, or orofacial myofunctional disorder, including abnormal fronting (tongue thrust) of the tongue at rest and during swallowing, lip incompetency, and sucking habits, can be identified reliably. Treatment Speech-language pathologists provide structural assessment including observation of face, jaw, lips, tongue, teeth, hard palate, soft palate, and pharynx, as well as perceptual and instrumental diagnostic procedures to assess oral and nasal airway functions as they pertain to orofacial myofunctional patterns, swallowing, and/or speech production. Neurological Motor Speech Disorder (See also Neurological Motor Speech Treatment, Apraxia, Dysarthria) Neurological motor speech assessment looks at the structure and function of the oral motor mechanism for non-speech and speech activities including assessment of muscle tone, muscle strength, motor steadiness and speech, range, and accuracy of motor movements. Treatment Intelligibility of speech is improved by increasing respiratory support for speech; improving laryngeal function and subsequent pitch, loudness, and voice quality; managing velopharyngeal inadequacy; normalizing muscle tone; and increasing muscle strength of the oral motor structures. Treatment also focuses on improving accuracy, precision, timing, and coordination of articulation; implementing rate modification; and improving prosody and naturalness of speech. Therapy that incorporates a variety of techniques, including relaxed-throat breathing, has been shown to improve symptoms of vocal cord dysfunction and reduce recurrences (Doshi & Weinberger, 2006; Pargeter & Mansur, 2006). These disorders are typically characterized by speech and voice that are monotonous, quiet, hoarse, and breathy. These disabilities tend to increase as the disease progresses and can lead to serious problems with communication and swallowing. Intensive voice treatment protocols have been demonstrated to be effective in improving voice in this population (Sapir, Ramig & Fox, 2011). Speech-Language Pathology Medical Review Guidelines 47 Social Communication Disorder (See also Language Disorder, Language Treatment) Social communication disorders may include problems with social interaction, social cognition, and pragmatics (the social use of language). Social communication behaviors include eye contact, facial expressions, body language, and emotional expression. Treatment programs include both direct and indirect ways to mediate social exchanges. Instruction, modeling, role-play, and use of cognitive and behavioral learning principles to shape and encourage desired behaviors are all treatment methods. Studies support treatment, for example, of 10 studies reviewed, seven (70%) reported positive treatment effects and three of the 10 studies (30%) reported no treatment efficacy (Rao, et al. Speech Sound Disorders (Articulation Disorder, Phonological Process Disorder; See also Speech Sound Disorders Treatment) Speech sound impairments may arise from problems with articulation (making sounds) and phonological processes (sound patterns). Articulation disorders include problems with articulation and may involve sound substitutions, omissions, additions, or distortions. For example, sounds made in the back of the mouth like "k" and "g" may be substituted for those in the front of the mouth like "t" and "d". Treatment Speech sound disorders treatment focuses on correct speech sound production. Treatment optimizes speech discrimination, speech sound production, and intelligibility in multiple communication contexts. Stuttering and Cluttering Disorder (See also Fluency Treatment) Stuttering (stammering) is a speech disorder in which sounds, syllables, or words are repeated or prolonged, disrupting the normal flow of speech. These speech disruptions may be accompanied by struggling behaviors, such as rapid eye blinks or tremors of the lips. Stuttered speech often includes repetitions of words or parts of words, as well as prolongations of speech Speech-Language Pathology Medical Review Guidelines 48 sounds. Speech may become completely stopped or blocked, so that the mouth is positioned to say a sound, sometimes for several seconds, with little or no sound forthcoming. Cluttering is a syndrome characterized by a speech delivery rate that is abnormally fast and/or irregular. Cluttered speech is characterized by one or more of the following: (1) failure to maintain normally expected sound, syllable, phrase, and pausing patterns and/or (2) greater than expected incidents of dysfluency, the majority of which are unlike those typical of people who stutter. Examples of cluttered speech include compressed consonant clusters, unfinished words, and shortened vowels. Treatment Current therapies for individuals who stutter focus on learning ways to minimize stuttering that include speaking more slowly, regulating breathing, or gradually progressing from singlesyllable responses to longer words and more complex sentences. Easy onset of voicing, light articulatory contacts, and use of computer-assisted feedback to train the patient in fluency are treatment methods designed to establish fluent speech. Fluency intervention is provided to improve aspects of speech fluency and concomitant features of fluency disorders to optimize activity/participation, such as reduction of avoidance behaviors. Communication requires a complex interplay between cognition, language, and speech, with cognitive processes ranging from basic to complex and includes attention, memory, reasoning, and executive functions. Communication involves listening, reading, writing, speaking, and gesturing at all levels of language. Treatment Intervention is tailored to the unique needs of the individual and may focus on such skills as attention, memory, pragmatics, problem solving, and functional communication. The goal of cognitive-communication intervention is for the person to achieve the highest possible level of communicative participation in daily living. Velopharyngeal Dysfunction (See also Cleft Lip and Palate, Voice and/or Resonance Treatment, Voice and/or Resonance Disorder) the purpose of the velopharyngeal mechanism is to close off the nasal cavity from the oral cavity during speech, normalizing both resonance and articulation for pressure sensitive phonemes. Instrumentation may be used to assess this problem (see Speech-Language Pathology Instrumentation). Resonance can be assessed as normal, hypernasal, hyponasal, or mixed hyper/hyponasal. If a cleft palate/craniofacial team is involved, for example, team members will have access to: a nasometer that analyzes acoustic energy emitted through the oral cavity and nasal cavity during the production of speech aerodynamic assessment, measuring oral pressure and oral airflow during speech, and estimating the size of the velopharyngeal gap/orifice nasopharyngoscopy (a procedure using a flexible fiberoptic nasopharyngeal scope) to visualize the velopharyngeal mechanism and its function by viewing the nasal surface of the velum and the velopharyngeal port during connected speech videofluoroscopy and lateral cephalographs to assess velopharyngeal closure during speech and phonation, respectively. Speech-Language Pathology Medical Review Guidelines 50 Treatment Improving articulatory placement and eliminating compensatory errors to improve velopharyngeal function and decrease the perception of hypernasality may be a focus of treatment. Eliminating inappropriate velopharyngeal patterns by looking, listening, and feeling for nasal air flow using auditory feedback, tactile feedback, and visual feedback may also be a focus of treatment. Voice and/or Resonance Disorder (See also Velopharyngeal Dysfunction, Cleft Lip and Palate, Voice and/or Resonance Treatment; Laryngectomy) Voice disorder, or dysphonia (an impairment of the speaking voice), arises from an abnormality of the structures and or functions of the voice production system and can cause bodily pain, a personal communication disability, and an occupational or social handicap. Genetic factors may predispose an individual to voice disorders; chronic and acute variables such as occupational vocal demands, medications, health problems, environment, physical trauma, and lifestyle choices may precipitate dysphonia. Loudness is the perceived volume (or amplitude) of the sound; quality refers to the distinctive attributes of a sound. Treatment is provided for individuals with resonance or nasal airflow disorders, velopharyngeal incompetence, or articulation disorders caused by velopharyngeal incompetence and related disorders such as cleft lip/palate. In complex disorders, such as paradoxical vocal fold motion, voice therapy helps to reduce longterm costs of treatment by minimizing expensive emergency room visits and hospitalizations. Benign vocal fold lesions are a common cause of dysphonia, and most laryngologists consider voice therapy, often together with medical management, the initial treatment of choice for benign lesions. Many studies have documented excellent outcomes after voice therapy in patients with a variety of benign lesions (Blood, 1994; Gordon, Pearson, Paton, & Montgomery, 1997; Holmberg, Hillman, Hammarberg, Sodersten, & Doyle, 2001; Lancer, Snyder, Jones, & Le Boutillier, 1988; McCrory, 2001; Murry & Woodson, 1992; Smith & Thyme, 1976; Speyer, Weineke, Hosseini, Kempen, Kersing, & DeJonckere, 2002. Increasingly, otolaryngologists are using Speech-Language Pathology Medical Review Guidelines 51 response to voice therapy to help differentiate among benign mucosal lesions, inform the treatment decision for surgery, and optimize surgical outcome. When surgery is necessary, preand postoperative voice therapy may shorten the postoperative recovery time, allowing faster return to work and limiting scar tissue and permanent dysphonia. Most otolaryngologists consider voice therapy essential as definitive treatment or as adjunctive to surgery for patients with unilateral vocal fold paralysis (Benninger et al. Evidence suggests that preoperative voice therapy improves voice outcomes for greater than 50% of patients with unilateral vocal fold paralysis and may render surgery unnecessary (Heuer, et al. See also Voice and Resonance Instrumentation under Voice and/or Resonance Treatment. The final analysis and interpretation of an instrumental assessment should include a definitive diagnosis, identification of the swallowing phase(s) affected, and a recommended treatment plan, including compensatory swallowing techniques and/or postures and food and/or fluid texture modification. An instrumental assessment is not indicated if findings from the clinical evaluation fail to support a suspicion of dysphagia or if they suggest dysphagia but (1) the patient is unable to cooperate or participate in an instrumental evaluation or (2) the instrumental examination would not change the clinical management of the patient. The effects of compensatory maneuvers and diet modification on aspiration prevention and/or bolus transport during Speech-Language Pathology Medical Review Guidelines 55 swallowing can be studied radiographically to determine a safe diet and to maximize efficiency of the swallow. Therapeutic maneuvers are attempted during this examination to determine a safe diet and to maximize the efficiency of the swallow. Individuals of all ages are treated on the basis of swallowing function assessment. At the conclusion of the assessment, the presence, severity, and pattern of dysphagia should be determined, and recommendations made with collaboration among the therapist, physician, and patient/family. Electrolarynx An electrolarynx is a handheld device held against the throat region (or mouth with an oral adapter immediately post-op) to provide vibrations that allow speech sound. Instrumental techniques ensure the validity of signal processing, analysis routines, and elimination of task or signal artifacts. If a cleft palate/craniofacial team is involved, for example, team members will have access to: a nasometer that analyzes acoustic energy emitted through the oral cavity and nasal cavity during the production of speech aerodynamic assessment, measuring oral pressure and oral airflow during speech, and estimating the size of the velopharyngeal gap/orifice Speech-Language Pathology Medical Review Guidelines 56 nasopharyngoscopy (a procedure using a flexible fiberoptic nasopharyngealscope) to visualize the velopharyngeal mechanism and its function by viewing the nasal surface of the velum and the velopharyngeal port during connected speech videofluoroscopy and lateral cephalographs to assess velopharyngeal closure during speech and phonation, respectively. Videostroboscopic laryngoscopy incorporates a stroboscope, laryngeal fiberscope, and videoscope to produce a permanent image of the motion of the vocal folds. Videostroboscopy is a diagnostic procedure for examination of the vocal cords when pathology is suspected (based on persistent symptoms or other findings with suspected pathology such as carcinoma, vocal cord paralysis, or polyps) despite a negative or unsatisfactory/inadequate mirror-image and endoscopic examinations. Speech-Language Pathology Prosthetics Intervention services are conducted to help individuals to understand, use, adjust, and restore their customized prosthetic/adaptive devices. Tracheostomy Speaking Valves Tracheostomy speaking valves such as the Passy-Muir valve are considered voice prosthetics that enable the wearer to produce speech. As such, speaking valves that restore more normal phonation are often key tools in the effort to restore speech and promote more typical language development in this population"(Hoffman, Bolton, & Ferry, 2008). Tracheotomized patients, both adults and children, use tracheostomy speaking valves. Cochlear Implants Cochlear Implants are small, complex electronic devices that help to provide a sense of sound to a person who is profoundly deaf or severely hard-of-hearing. Cochlear implants, coupled with intensive post-implantation therapy, can help young children to acquire speech, language, and social skills and, in adult implant patients, facilitate sound awareness, increased speech, and environmental sound detection. Cochlear implants enable sound to transmit to the auditory nerve so that profoundly hearing impaired or entirely deaf patients can process sounds.
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Hepatic candidiasis results from seeding of the liver during neutropenia in pts with hematologic malignancy but presents when neutropenia resolves medicine 4 the people purchase primaquine 7.5 mg with mastercard. Pts have fever symptoms 4dp3dt cheap primaquine 15mg visa, right lower quadrant tenderness treatment 3rd degree burns primaquine 15 mg discount, and diarrhea that is often bloody medicine 968 discount 7.5 mg primaquine mastercard. Splenectomized pts and those with hypogammaglobulinemia are also at risk for infection with encapsulated bacteria such as Streptococcus pneumoniae medications dispensed in original container generic primaquine 7.5 mg fast delivery, Haemophilus influenzae medications for bipolar buy 7.5 mg primaquine with mastercard, and Neisseria meningitidis. Candida has a predilection for the kidneys, reaching this site via either hematogenous seeding or retrograde spread from the bladder. Obvious infectious site found No obvious infectious site Follow-up Subsequent therapy Treat the infection with the best available antibiotics. The development of fever in a pt receiving antibiotics affects the choice of subsequent therapy (which should target resistant organisms and organisms known to cause infections in pts being treated with the antibiotics already administered). Outpatients who are expected to remain neutropenic for <10 days and who have no concurrent medical problems (such as hypotension, pulmonary compromise, or abdominal pain) can be classified as low-risk and treated with a broad-spectrum oral regimen. Approach to Diagnosis and Treatment of Febrile Neutropenic Pts Figure 86-1 presents an algorithm for the diagnosis and treatment of febrile neutropenic pts. Adding antibiotics to the initial regimen is not appropriate unless there is a clinical or microbiologic reason to do so. Severe disease is more common among allogeneic transplant recipients and is often associated with graftversus-host disease. However, the transplant recipient is often better equipped to combat late infection as a result of improved graft function and, in many cases, less intense immunosuppression. Late infections (>6 months): Listeria, Nocardia, various fungi, and other intracellular organisms associated with defects in cell-mediated immunity may pose problems. Reduction of the degree of immunosuppression is critical to reduce rates of graft loss. Pertussis vaccines have not been recommended for people >6 years of age in the past. However, recent data indicate that the Tdap (tetanus-diphtheria-acellular pertussis) product is both safe and efficacious in adults. It is anticipated that future vaccines will include more serotypes and will be recommended for adults. Fungal infections are common and correlate with preoperative glucocorticoid use or long-term antimicrobial use. Solid organ transplant recipients receiving immunosuppressive agents should not receive live vaccines. For a more detailed discussion, see Finberg R: Infections in Patients with Cancer, Chap. The incidence of endocarditis is increased among the elderly and among pts with prosthetic heart valves. The risk of endocarditis is greatest during the first 6 months after valve replacement. Streptococcus bovis originates from the gut and is associated with colon polyps or cancer. Nosocomial endocarditis, frequently due to Staphylococcus aureus, arises most often from bacteremia related to intravascular devices. Emboli most commonly arise from vegetations >10 mm in diameter and from those located on the mitral valve. With antibiotic treatment, the frequency of emboli decreases from 13 per 1000 pt-days during the first week of infection to 1. Tricuspid Valve Endocarditis this condition is associated with fever, faint or no heart murmur, and prominent pulmonary findings such as cough, pleuritic chest pain, and nodular pulmonary infiltrates. Definite endocarditis is defined by 2 major, 1 major plus 3 minor, or 5 minor criteria. The erythrocyte sedimentation rate, C-reactive protein level, and circulating immune complex titer are typically elevated. Evidence of endocardial involvement Positive echocardiograma Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation, or Abscess, or New partial dehiscence of prosthetic valve, or New valvular regurgitation (increase or change in preexisting murmur not sufficient) Minor Criteria 1. Microbiologic evidence: positive blood culture but not meeting major criterion as noted previouslyb or serologic evidence of active infection with organism consistent with infective endocarditis echocardiography is recommended for assessing possible prosthetic valve endocarditis or complicated endocarditis. Pts treated with vancomycin or an aminoglycoside should have serum drug levels monitored. Ideal body weight is used to calculate doses of gentamicin and streptomycin per kilogram (men = 50 kg + 2. Groups B, C, and G streptococcal endocarditis should be treated with the regimen recommended for relatively penicillinresistant streptococci (Table 87-2). If treatment fails or the isolate is resistant to commonly used agents, surgical therapy is advised (see below and Table 87-3). Two other agents in addition to rifampin help prevent the emergence of rifampin resistance in vivo. Susceptibility testing for gentamicin should be performed before rifampin is given; if the strain is resistant, another aminoglycoside or a fluoroquinolone should be substituted. If the pt has a prosthetic valve, those two drugs plus vancomycin should be given. Ruptured mycotic aneurysms should be clipped and cerebral edema allowed to resolve prior to cardiac surgery. Table 87-4 lists the high-risk cardiac lesions for which prophylaxis is advised, and Table 87-5 lists the recommended antibiotic regimens for this purpose. Primary peritonitis has no apparent source, whereas secondary peritonitis is caused by spillage from an intraabdominal viscus. Although some pts experience an acute onset of abdominal pain or signs of peritoneal irritation, other pts have only nonspecific and nonlocalizing manifestations. Enteric gram-negative bacilli such as Escherichia coli or gram-positive organisms such as streptococci, enterococci, and pneumococci are the most common etiologic agents; a single organism is typically isolated. Culture yield is improved if 10 mL of peritoneal fluid is placed directly into blood culture bottles. Infection almost always involves a mixed aerobic and anaerobic flora, especially when the contaminating source is colonic. Once infection has spread to the peritoneal cavity, pain increases; pts lie motionless, often with knees drawn up to avoid stretching the nerve fibers of the peritoneal cavity. The selected antibiotics are aimed at aerobic gram-negative bacilli and anaerobes-e. Several hundred milliliters of removed dialysis fluid should be centrifuged and sent for culture, preferably in blood culture bottles to improve the diagnostic yield. Empirical therapy should be directed against staphylococcal species and gram-negative bacilli. Antimicrobial therapy is adjunctive to drainage and/or surgical correction of an underlying lesion or process, although diverticular abscesses usually wall off locally and surgical intervention is not routinely needed. Antimicrobial agents with activity against gram-negative bacilli and anaerobic organisms are indicated (see "Secondary Peritonitis," above). Amebic liver abscesses are not uncommon; amebic serology has yielded positive results in >95% of affected pts. Drainage remains the mainstay of treatment, but medical management with long courses of antibiotics can be successful. Splenic Abscess Splenic abscesses usually develop by hematogenous spread of infection. Abdominal pain or splenomegaly occurs in ~50% of cases and pain localized to the left upper quadrant in ~25%. Gram-negative bacilli can cause splenic abscess in pts with urinary tract foci, and Salmonella can be responsible in pts with sickle cell disease. Pts with multiple or complex multilocular abscesses should undergo splenectomy, receive adjunctive antibiotics, and be vaccinated against encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis). Perinephric and Renal Abscesses More than 75% of these abscesses are due to ascending infection and are preceded by pyelonephritis. Treatment includes drainage and the administration of antibiotics active against the organisms recovered. The wide range of clinical manifestations is matched by the wide variety of infectious agents involved (Table 89-1). On physical examination, particular attention to signs of dehydration and abdominal findings is warranted. Disease lasts <12 h and consists of diarrhea, nausea, vomiting, and abdominal cramping, usually without fever. Infection requires ingestion of a relatively large inoculum (compared with other pathogens). A single dose of an antibiotic can be used in conjunction: doxycycline (300 mg), ciprofloxacin (30 mg/kg, not to exceed 1 g), or azithromycin (1 g). In the United States, >90% of outbreaks of nonbacterial gastroenteritis are caused by noroviruses. Infections with Noroviruses and Related Human Caliciviruses Only supportive measures are required. Vomiting often precedes diarrhea (loose, watery stools without blood or fecal leukocytes), and about one-third of pts are febrile. Disease in developing countries occurs in younger children and is more severe than in industrialized countries; further study is needed before global recommendations for vaccine use can be issued. Cysts are ingested from the environment, excyst in the small intestine, and release flagellated trophozoites. People at the extremes of age, those newly exposed, and pts with hypogammaglobulinemia are at increased risk-a pattern suggesting a role for humoral immunity in resistance. Diagnosis Giardiasis can be diagnosed by parasite antigen detection in feces and/or examination of several samples from freshly collected stool specimens, with concentration methods used to identify cysts (oval, with four nuclei) or trophozoites (pear-shaped, flattened parasites with two nuclei and four pairs of flagella). In cases of treatment failure, document continued infection before re-treatment, and seek possible sources of reinfection. Person-to-person transmission of infectious oocysts can occur among close contacts and in day-care settings. Nontyphoidal salmonellae most commonly cause gastroenteritis, invading the large- and small-intestinal mucosa and resulting in massive polymorphonuclear leukocyte infiltration. Disease results from ingestion of contaminated food or water and is rare in developed nations. Physical findings include rash ("rose spots"), hepatosplenomegaly, epistaxis, and relative bradycardia. Nontyphoidal salmonellosis: the incidence of nontyphoidal salmonellosis in the United States is 14. The main mode of transmission is from contaminated food products, such as eggs (S. Diarrhea is usually loose, nonbloody, and moderate in volume, but stools are sometimes bloody. Diagnosis Positive cultures of blood, stool, or other specimens are required for diagnosis. If blood cultures are positive for nontyphoidal salmonellae, highgrade bacteremia should be ruled out by obtaining multiple blood cultures. However, infants, the elderly, the immunosuppressed, and pts with cardiac, valvular, or endovascular abnormalities may require antibiotic treatment. Pts with endovascular infections or endocarditis should receive 6 weeks of treatment with a third-generation cephalosporin.
Invasive bacterial infections are a prominent cause of death around the world medications used to treat bipolar disorder discount primaquine 7.5 mg line, especially among young children medicine reminder app discount primaquine 15 mg on line. In sub-Saharan Africa medications hydroxyzine order primaquine 15mg online, at least onequarter of deaths of children >1 year of age are due to community-acquired bacteremia symptoms stomach cancer buy primaquine 7.5 mg mastercard. Although blood flow to peripheral tissues increases symptoms 0f parkinson disease primaquine 15mg generic, oxygen utilization by these tissues is greatly impaired medicine kit for babies order primaquine 7.5mg online. Sepsis and Septic Shock Patients in whom sepsis is suspected must be managed expeditiously, if possible within 1 h of presentation. If the local prevalence of cephalosporin-resistant pneumococci is high, add vancomycin. If the pt is allergic to -lactam drugs, ciprofloxacin (400 mg q12h) or levofloxacin (750 mg q12h) plus vancomycin (15 mg/kg q12h) plus tobramycin should be used. General support: Nutritional supplementation should be given to pts with prolonged sepsis. Tight control of blood glucose levels in pts who have just undergone major surgery may improve survival rates. Other risk factors include older age, chronic alcohol abuse, metabolic acidosis, and overall severity of critical illness. Exudative phase-Characterized by alveolar edema and leukocytic inflammation, with subsequent development of hyaline membranes from diffuse alveolar damage. The alveolar edema is most prominent in the dependent portions of the lung; this causes atelectasis and reduced lung compliance. The differential diagnosis is broad, but common alternative etiologies to consider are cardiogenic pulmonary edema, pneumonia, and alveolar hemorrhage. Proliferative phase-This phase can last from approximately days 7 to 21 after the inciting insult. Although most pts recover, some will develop progressive lung injury and evidence of pulmonary fibrosis. Even among pts who show rapid improvement, dyspnea and hypoxemia often persist during this phase. Hypoxemic respiratory failure is defined by arterial O2 saturation <90% while receiving an inspired O2 fraction >0. Acute hypoxemic respiratory failure can result from pneumonia, pulmonary edema (cardiogenic or noncardiogenic), and alveolar hemorrhage. Hypoxemia results from ventilation-perfusion mismatch and intrapulmonary shunting. Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Various modes of mechanical ventilation are commonly used; different modes are characterized by a trigger (what the ventilator senses to initiate a machine-delivered breath), a cycle (what determines the end of inspiration), and limiting factors (specified values for key parameters that are monitored by the ventilator and not allowed to be exceeded). If no effort is detected over a prespecified time interval, a timer-triggered machine breath is delivered. Limiting factors include the minimum respiratory rate, which is specified by the operator; pt efforts can lead to higher rates. Because the pt will receive a full tidal breath with each inspiratory effort, tachypnea due to nonrespiratory drive (such as pain) can lead to respiratory alkalosis. As with Assist-control, the trigger for a machine-delivered breath can be either pt effort or a specified time interval. The level of inspiratory pressure is an operator-specified limiting factor in this mode of ventilation; the achieved tidal volume and inspiratory flow rate result from this prespecified pressure limit, and a specific tidal volume or minute ventilation may not be achieved. After an endotracheal tube has been in place for an extended period of time, tracheostomy should be considered, primarily to improve pt comfort and management of respiratory secretions. No absolute time frame for tracheostomy placement exists, but pts who are likely to require mechanical ventilatory support for >3 weeks should be considered for a tracheostomy. Barotrauma, overdistention and damage of lung tissue, typically occurs at high airway pressures (>50 cmH2O). Ventilator-associated pneumonia is a major complication of mechanical ventilation; common pathogens include Pseudomonas aeruginosa and other gram-negative bacilli, as well as Staphylococcus aureus. Assessment should determine whether there is a change in level of consciousness (drowsy, stuporous, comatose) and/or content of consciousness (confusion, perseveration, hallucinations). Confusion is a lack of clarity in thinking with inattentiveness; delirium is used to describe an acute confusional state; stupor, a state in which vigorous stimuli are needed to elicit a response; coma, a condition of unresponsiveness. Patients in such states are usually seriously ill, and etiologic factors must be assessed (Tables 17-1 and 17-2). Observation will usually reveal an altered level of consciousness or a deficit of attention. Delirium is vastly underrecognized, especially in pts presenting with a quiet, hypoactive state. A cost-effective approach to the evaluation of delirium allows the history and physical exam to guide tests. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria, Waterhouse-Friderichsen syndrome d. Miscellaneous: Fat embolism, cholesterol embolism, carcinomatous and lymphomatous meningitis, etc. Management of the delirious pt begins with treatment of the underlying inciting factor. Relatively simple methods of supportive care can be quite effective, such as frequent reorientation by staff, preservation of sleep-wake cycles, and attempting to mimic the home environment as much as possible. Chemical restraints exacerbate delirium and should be used only when necessary to protect pt or staff from possible injury; antipsychotics at low dose are usually the treatment of choice. Immediate Assessment Acute respiratory and cardiovascular problems should be attended to prior to the neurologic assessment. Thiamine, glucose, and naloxone should be administered if the etiology of coma is not immediately apparent. Multifocal myoclonus indicates that a metabolic disorder is likely; intermittent twitching may be the only sign of a seizure. Pupillary Signs In comatose pts, equal, round, reactive pupils exclude midbrain damage as cause and suggest a metabolic abnormality. Pinpoint pupils occur in narcotic overdose (except meperidine, which causes midsize pupils), pontine damage, hydrocephalus, or thalamic hemorrhage; the response to naloxone and presence of reflex eye movements (usually intact with drug overdose) can distinguish these. Vertical separation of ocular axes (skew deviation) occurs in pontine or cerebellar lesions. Cheyne-Stokes (periodic) breathing occurs in bihemispheric dysfunction and is common in metabolic encephalopathies. The pt is unresponsive to all forms of stimulation (widespread cortical destruction), brainstem reflexes are absent (global brainstem damage), and there is complete apnea (destruction of the medulla). The absence of deep tendon reflexes is not required because the spinal cord may remain functional. Much can be done to limit morbidity and mortality through prevention and acute intervention. Small, deep ischemic lesions are most often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are seen with severe proximal stenosis and inadequate collaterals challenged by systemic hypotensive episodes. Variability in stroke recovery is influenced by collateral vessels, blood pressure, and the specific site and mechanism of vessel occlusion; if blood flow is restored prior to significant cell death, the pt may experience only transient symptoms, i. Pts may not seek assistance on their own because they are rarely in pain and may lose appreciation that something is wrong (anosagnosia). Intracranial Hemorrhage Vomiting and drowsiness occur in some cases, and headache in about one-half. Stroke needs to be distinguished from potential mimics, including seizure, migraine, tumor, and metabolic derangements. Treatments designed to reverse or lessen tissue infarction include: (1) medical support, (2) thrombolysis and endovascular techniques, (3) antiplatelet agents, (4) anticoagulation, and (5) neuroprotection. Intravascular volume should be maintained with isotonic fluids as volume restriction is rarely helpful. Osmotic therapy with mannitol may be necessary to control edema in large infarcts, but isotonic volume must be replaced to avoid hypovolemia. Only a small percentage of stroke pts are seen early enough to receive treatment with these techniques. Neuroprotection Hypothermia is effective in coma following cardiac arrest but has not been adequately studied in pts with stroke. Neurosurgical consultation should be sought for possible urgent evacuation of cerebellar hematoma; in other locations, data do not support surgical intervention. Clinical examination should be focused on the peripheral and cervical vascular system. If a hypercoagulable state is suspected, further studies of coagulation are indicated. Hypertension and diabetes are also specific risk factors for lacunar stroke and intraparenchymal hemorrhage. Embolic Stroke In pts with atrial fibrillation, the choice between warfarin or aspirin prophylaxis is determined by age and risk factors; the presence of any risk factor tips the balance in favor of anticoagulation (Table 18-6). For prosthetic heart valve pts, a combination of aspirin and warfarin may be indicated depending on the type and location of the prosthetic valve. Anticoagulation Therapy for Noncardiogenic Stroke Data do not support the use of long-term warfarin for preventing atherothrombotic stroke for either intracranial or extracranial cerebrovascular disease. Surgical Therapy Carotid endarterectomy benefits many pts with symptomatic severe (>70%) carotid stenosis; the relative risk reduction is ~65%. However, if the perioperative stroke rate is >6% for any surgeon, the benefit is lost. Clinical Presentation Sudden, severe headache, often with transient loss of consciousness at onset; vomiting is common. A progressive third nerve palsy, usually involving the pupil, along with headache suggests posterior communicating artery aneurysm. In addition to dramatic presentations, aneurysms can undergo small ruptures with leaks of blood into the subarachnoid space (sentinel bleeds). Subarachnoid Hemorrhage Aneurysm Repair Early aneurysm repair prevents rerupture and allows the safe application of techniques used to improve blood flow should symptomatic vasospasm develop. Anticonvulsants may be begun at diagnosis and continued at least until the aneurysm is treated, although some experts reserve this therapy only for patients in whom a seizure has occurred. Blood pressure should be carefully controlled initially, while preserving cerebral blood flow, in order to decrease the risk of rerupture until the aneurysm is repaired. Vasospasm Symptomatic vasospasm is the leading cause of mortality and morbidity following initial rupture; may occur by day 4 and continue through day 14, leading to focal ischemia and possibly stroke. Cerebral perfusion can be improved in symptomatic vasospasm by increasing mean arterial pressure with vasopressor agents such as phenylephrine or norepinephrine, and intravascular volume can be expanded with crystalloid, augmenting cardiac output and reducing blood viscosity by reducing the hematocrit; this so-called "triple-H" (hypertension, hemodilution, and hypervolemic) therapy is widely used. If symptomatic vasospasm persists despite optimal medical therapy, intraarterial vasodilators and angioplasty of the cerebral vessels can be effective. If not controlled, then cerebral hypoperfusion, pupillary dilation, coma, focal neurologic deficits, posturing, abnormal respirations, systemic hypertension, and bradycardia may result. Brain tissue is pushed away from the mass against fixed intracranial structures and into spaces not normally occupied. Posterior fossa masses, which may initially cause ataxia, stiff neck, and nausea, are especially dangerous because they can both compress vital brainstem structures and cause obstructive hydrocephalus. In head trauma and stroke, cytotoxic edema may be most responsible, and the use of osmotic diuretics such as mannitol becomes an appropriate early step. Hyperventilation is best used for only short periods of time until a more definitive treatment can be instituted. Emergency surgical intervention is sometimes necessary to decompress the intracranial contents. Hydrocephalus, cerebellar stroke with edema, surgically accessible tumor, and subdural or epidural hemorrhage often require lifesaving neurosurgery. If transient and unaccompanied by other serious brain pathology other than a short period of amnesia, it is called concussion. Glucocorticoids-dexamethasone 4 mg q6h for vasogenic edema from tumor, abscess (avoid glucocorticoids in head trauma, ischemic and hemorrhagic stroke) 5. Cerebral blood flow and microdialysis probes (not shown) may be placed in a manner similar to the brain tissue oxygen probe. Minor Concussive Injury the pt with minor head injury who is alert and attentive after a short period of unconsciousness (<1 min) may have headache, dizziness, faintness, nausea, a single episode of emesis, difficulty with concentration, or slight blurring of vision. Such patients have usually sustained a concussion and are expected to have a brief amnestic period.