Paul W Ladenson, M.D.

• John Eager Howard Professor of Endocrinology & Metabolism
• Professor of Medicine

https://www.hopkinsmedicine.org/profiles/results/directory/profile/0002745/paul-ladenson

Patterns of serum gonadal steroid concentrations in man from birth to 2 years of age anxiety yoga poses order genuine venlor on line. Androgen insensitivity syndrome: Long-term medical anxiety symptoms ringing in ears purchase venlor 75 mg free shipping, surgical and psychosexual outcome anxiety coach order venlor mastercard. The conceptual domain involves academic competence anxiety 6 months after giving birth order venlor 75 mg mastercard, the acquisition of practical knowledge anxiety symptoms joins bones purchase 75 mg venlor fast delivery, and judgment in novel situations anxiety symptoms in cats order 75mg venlor overnight delivery. However, they reported higher rates of psychologic distress and lower rates of participation in formal organizations. These conditions begin during childhood (before 22 years of age), and interfere with mobility, acquisition of self-care ability, communication skills, social skills, general learning ability, and independent living. Developmental disabilities may be isolated, as in a child with impaired vision, or may be multiple, as in a child with delays in motor, cognitive, language, and social functioning. Some etiologies are fully or partly amenable to early educational and medical interventions, while others may lead to permanent intellectual impairment or progressive deterioration of functioning. For example, standardized tests of intelligence have a mean of 100 and standard deviation of 15 points. Developmental Disability Developmental disabilities affect approximately 1 in 6 children in the United States (13. From a community perspective, having a specific diagnosis for an affected individual helps in the development of treatment and prevention strategies. In addition, the origin of developmental disability is not apparent in many children, or there may be multiple possible causal factors or multiple disabilities present. For example, 23% of children with developmental disabilities have 2 disabilities, and 6% have 3 or more. Boys have more than twice the prevalence of any developmental disability, and children insured by Medicaid have a nearly 2-fold higher prevalence of disability compared with those with private insurance. The overall prevalence of disability increased by 17% between 1997 and 2008, mostly due to a nearly 4-fold change in autism (from 0. In addition, newborn screening programs may identify children with rare but significant problems who require early treatments and interventions. For example, it has been shown that low 5-minute Apgar scores, in the absence of other symptoms of neonatal encephalopathy, correlate poorly with long-term neurologic dysfunction. Sociocultural risks also can have profound effects on development and may interact with biologic risk factors to create a greater effect than any single factor alone (so-called "double jeopardy"). For example, barring catastrophic circumstances, child-rearing conditions that support and enrich early development may compensate for biologic deficits. Sociocultural factors, such as small family size, higher level of parental education, and fewer changes in residence have a more powerful positive effect than many biologic risks and seem to be important predictors of developmental functioning beyond infancy. The brains of infants and young children are remarkably resilient and normal cognitive and language outcomes are often seen, even in the face of perinatal stroke or similar focal brain injuries. In addition, preschool early intervention programs that are designed to mitigate the factors that place children at risk for poor outcomes have been shown to have significant short- and long-term educational, behavioral, and economic benefits (Table 24. All neonates should routinely undergo an evaluation of their fundi for the presence of a red reflex, which can be obscured by cataract or tumor, as well as inspection of the globe, which may be affected by congenital glaucoma. Infants with nystagmus who do not follow visually by 3 months of age, who have dissociation between visual behavior and motor behavior, or whose parents express concern about their vision should undergo a formal ophthalmologic evaluation. Loss of Hearing Early detection of hearing loss is critical for optimizing the language development of these children. More than 95% of all children born in the United States are screened for hearing loss shortly after birth. Although the prevalence of congenital deafness is low in the general population (1-3/1,000 infants), it is higher in infants who require neonatal intensive care services (2-4/100 infants). They would not receive hearing intervention within the 1st 6 months of life, a period that is critical for speech, language, and later learning development. A number of genetic syndromes are associated with deafness (Waardenburg, Alport, Pendred, and Jervell and LangeNielsen) and progressive or late-onset hearing loss can occur in neurofibromatosis, Usher syndrome, Hunter syndrome, Friedreich ataxia, or Charcot-Marie-Tooth syndrome (Table 24. In addition, parental concern about hearing loss has a sensitivity of approximately 44%. Deaf infants may smile, coo, and babble; however, their vocalizations usually cease after 8 months of age. The traditional screening takes the form of biochemical and ultrasound tests, which may detect fetuses at high risk for chromosome anomalies and neural tube defects. An abnormal result on these screenings is typically followed by highresolution ultrasonography, chorionic villus sampling or amniocentesis, genetic testing (chomosome analysis or microarray), and genetic counseling. These technologies identify possible chromosomal and microdeletion disorders through maternal blood screening. If an abnormality is detected, a confirmatory test is still required through more invasive techniques such as amniocentesis. In addition, prenatal genetic carrier screening can be performed for a large number of disorders; at present, these are the only standard of care for individuals at high risk for certain genetic conditions. Test samples should be collected between 24-48 hours of age, but results may be influenced by a variety of maternal and infant factors. For example, tests for congenital adrenal hyperplasia are sensitive to the weight of the infant and the use of steroids. While all states screen for a "core panel" of 29 conditions, they vary in testing for other conditions. Clinicians should familiarize themselves with the specific tests that are routinely performed in each state. Speech refers to the mechanics of oral communication (sound production); language includes the understanding, processing, and production of communication (words). Speech problems may include articulation (pronunciation) deficits (phonologic or apraxic speech disorders), fluency disorders (stuttering), or unusual voice quality. Language delays may be confined to expression with normal receptive abilities, or may involve both expressive and receptive abilities. Children with speech and language delays often experience emotional and social adjustment difficulties related to their inability to communicate effectively with parents and peers. In general, children with normal comprehension of language and normal nonverbal cognitive abilities have an excellent prognosis, while those with receptive delays are at risk for language-based learning disabilities (reading comprehension and writing disorders) (Table 24. Many disorders may not manifest until children are preschool or school age, and some infrequent disorders cause regression or deterioration of function beginning at different ages. Multiple studies have found parental concern to identify correctly 74-80% of preschool age children (0-6 years old) with cognitive delays, speech and language delays, and learning disabilities. Conversely, the absence of parental concern correctly identified 70-80% of children without a significant disability. Thus, reliance on parental concern alone as a means of identification (sensitivity and specificity) matches acceptable standards for more formal developmental screening tests. However, sole reliance on parental concerns will miss a substantial number of children with developmental concerns, especially those with more subtle disabilities, for a variety of reasons. In particular, children without obvious physical impairments may not be identified until they enter a formal school program. Complicating matters further, children with developmental disabilities may experience significant behavioral or emotional difficulties that "mask" (or distract from) their underlying developmental difficulties. Based on the findings from these evaluations, further subspecialty consultations. Many disabilities have their origin in the prenatal period, so the pregnancy and birth history are reviewed carefully for possible developmental risk factors (Table 24. Difficulty in conception or history of recurrent pregnancy loss may suggest the presence of an inherited chromosome anomaly. The method of delivery and the reason(s) for nonvaginal delivery may reflect on fetal status at the time of birth. Neonatal physical measurements (weight, length, and head circumference) when compared with gestational age are helpful in determining whether the child experienced intrauterine growth restriction. Severe medical complications in the neonatal period such as the presence of neonatal encephalopathy syndrome including seizures and multiorgan compromise, intraventricular hemorrhage, neonatal infections, prolonged requirement for mechanical ventilation, need for extracorporeal Developmental Screening Developmental screening involves the routine application of a brief standardized tool when there is no obvious concern. Developmental screening tests for use by health care providers have been available for several decades, but they are rarely administered by pediatricians, and generally lack sufficient sensitivity to identify subtle disorders while falsely identifying a significant number of nonaffected children. Instead, physicians are more likely to rely on their own clinical judgment, which detects fewer than 30% of children with significant developmental disabilities, or on informal and nonstandardized lists of developmental milestones. Developmental Surveillance Developmental surveillance is a "flexible, continuous process whereby knowledgeable professionals perform skilled observations of children throughout all encounters during child health care. To be effective, surveillance requires clinicians to be knowledgeable about child development and to recognize both variations of and deviations from normal patterns. At any point in this process, children who elicit concern about their development should be referred for further diagnostic evaluations and for early intervention and educational programs. Yes 5b Administer screening tool 6b Are the screening tool results positive/ concerning Yes 7 Make referrals for: Developmental and medical evaluations and early developmental intervention/early childhood services Action/process Decision Stop No Related evaluation and follow-up visits 8 Schedule next routine visit Developmental and medical evaluations Visit complete 10 Visit complete 9 Visit complete Schedule early return visit No Is a developmental disorder identified The social and economic circumstances of the family may reveal factors that place the infant at risk for developmental disabilities. The 1st weeks and months of life are a "transition period" for both the infant and the family. Children with developmental disabilities may begin to manifest symptoms in this period with difficulties nursing, excessive colic, poor weight gain, onset of seizures, or delayed achievement of motor milestones. Review of prior growth records may help differentiate between a congenital or acquired disorder. True regression, the loss of previously acquired skills, should be distinguished from failure of development. In cases of true regression, multiple areas of functioning are affected and do not reemerge over time. School experiences, academic readiness skills, educational achievement, and behavior patterns at home and school often reflect the cognitive and language development of school-age children and adolescents. Physical Examination the physical examination should begin with observations of the general appearance of the child, including overall state of health, visual and auditory responsiveness to the surroundings, and interactions with parents. When the child is at rest, subtle abnormalities of body proportions and movement patterns may be observed. Careful attention should also be paid to physical measurements (length/height, weight, and head circumference) with values plotted on standard reference curves. Both poor growth and excessive growth may be associated with metabolic disorders or genetic syndromes. Although large or small head size may be associated with significant pathology, a benign form of familial micro- and macrocephaly may be ruled out if 1 or both parents share the same trait. Dysmorphic features may suggest a recognizable pattern of deformation or malformation (Table 24. If the child has an unusual appearance, biologic family members should be examined either directly or from photographs to determine any resemblance. Additionally, examining serial photographs of a child at different ages can help to identify "coarsening" of facial features due to a storage disease (mucopolysaccharidosis). Abnormalities of skin pigmentation may suggest the presence of a neurocutaneous disorder (phakomatosis) associated with developmental disability (neurofibromatosis, tuberous sclerosis, Sturge-Weber syndrome) (see Chapter 30). Measurements of facial features, such as inner canthal distance, palpebral fissure length, auricular size and position, and development of the philtrum and upper lip, may be associated with structural anomalies of craniofacial development caused by genetic or teratogenic exposure (fetal alcohol syndrome). The oral structures should be examined for the presence of cleft palate (velocardiofacial syndrome, Stickler syndrome), macroglossia (Beckwith-Wiedemann syndrome), or recessed jaw (Pierre-Robin sequence). Anomalies of the neck may indicate vertebral abnormalities (Klippel-Feil syndrome) or genetic disorders (Turner syndrome, Noonan syndrome, Down syndrome). The abdominal exam may reveal evidence of an enlarged liver (associated with glycogen storage diseases, sphingolipidoses, or mucopolysaccharidoses). Examination of the back should include the "forward bend test" for scoliosis, and the presence of dimpling or a hirsute area in the lower spine that could represent an occult form of spinal dysraphism (tethered cord or other spinal cord anomaly). Anomalies of the extremities (limb proportions, hands, feet, and nails) are associated with a wide range of birth defects and syndromes. The presence of multiple malformations may be an important key to identifying a specific developmental disorder or syndrome. Although minor physical anomalies may be associated with developmental delay, most children with minor anomalies develop normally (Table 24. Ages of achievement of common milestones in motor, language, cognitive, and social development should be reviewed. It is important to know whether the child has received any type of educational or therapeutic interventions and the impact those programs have had on his or her behavior and development. The presence of 3 or more minor anomalies implies a greater chance that the child has a major anomaly and a diagnosis of a specific syndrome. Results of psychologic tests are not indicative of specific etiologies (genetic or acquired biologic conditions) and cannot determine whether a child has suffered a "brain injury," even in the context of a potentially traumatic event. Serial cognitive measures, particularly when there is premorbid information that has changed over time, may suggest the effects of trauma or a progressive disease process. The neuromotor examination should include observation of muscle bulk and presence or absence of muscle atrophy associated with myopathy. The assessment of cranial nerves includes evaluation for visual responsiveness, pupillary reactivity, presence of red reflexes, fullness of eye movements, and evidence of strabismus. Ptosis, asymmetry of facial expression, or abnormal tongue movement (deviation or fasciculation) suggests muscle weakness or partial paralysis. Muscle strength may be assessed by observing the child move about and manipulate objects. In the 1st year of life, motor milestones include the ability to sit independently, crawl, cruise, and walk. Decreased stretch reflex responsiveness may be due to lower motor neuron disease or myopathy. In infants, the persistence of primitive reflexes or the absence of protective postural reflexes is suggestive of neuromotor dysfunction. In older children, the presence of increased stretch reflexes, clonus, and positive Babinski reflexes are signs of upper motor neuron dysfunction associated with spasticity.

The other option involves instituting prednisone therapy to document that proteinuria has disappeared; this confirms the suspicion that the patient has steroid-responsive nephrotic syndrome anxiety 300mg purchase venlor uk. The rationale for withholding prednisone unless symptoms develop is that the natural history of minimal change disease is to remit; this may occur with or without prednisone administration anxiety shortness of breath generic venlor 75 mg on-line. If the patient has a more serious lesion anxiety symptoms concentration order venlor 75mg otc, symptoms will develop anxiety symptoms anger order venlor online, at which time evaluation and therapy may be undertaken anxiety symptoms of going crazy order venlor amex. In a patient older than 8 or 9 years anxiety symptoms cures cheap 75 mg venlor with mastercard, once the presence of persistent and nonorthostatic proteinuria is established, the next step is to quantify the amount of protein in a 24-hour specimen. If urinary protein excretion is greater than 8 mg/kg/day, a renal biopsy may be considered. Alternatively, these patients can also be treated with steroids and the response assessed. If proteinuria does not clear after 6-8 weeks of therapy, renal biopsy is then indicated. Hence, for an average 8-year-old patient who weighs 30 kg and is 1 m2 tall, proteinuria by these definitions is a level of 96 mg/day, and nephrotic syndrome is at a level of 960 mg/day. Renal biopsy can be considered at a Congenital Nephrotic Syndrome Congenital nephrotic syndrome is an autosomal recessive disorder resulting from mutations in the gene encoding the protein, nephrin (see Table 19. Infants with congenital nephrotic syndrome are often premature, with a low birthweight, placentomegaly, increased amniotic fluid -fetoprotein levels, and hypogammaglobinemia (decreased immunoglobulin G levels). Ascites and edema, caused by massive proteinuria, are usually present in affected infants during the first few weeks after birth. Infections and thrombosis are the two major complications; they cause considerable morbidity and mortality. Because of the massive proteinuria, patients fail to thrive; they require nasogastric feeding with a high-calorie, highprotein formula. Nephrectomy and peritoneal dialysis are often necessary to control protein losses and allow for adequate growth and control of uremia so that the infant can reach a size and nutritional state sufficient for renal transplantation. This has led to therapies that reduce proteinuria, thereby decreasing the risk of a progressive loss of renal function. The traffic of protein across the glomerular capillary membrane appears to stimulate a cascade of inflammatory events that cause interstitial fibrosis. This guideline helps avoid a biopsy for the patient with minimal proteinuria but does not require fullblown nephrotic syndrome to develop before a definitive work-up is initiated. However, the incidence of focal segmental sclerosis is much higher in adolescents than in younger children. Low molecular protein, such as 2-microblobulin, 1microglobulin, lysozyme, and retinol-binding protein can be seen in urine in tubular disorders, such as Fanconi syndrome or Dent disease. If associated with acidosis, hypokalemia, and hypophosphatemia, Fanconi syndrome should be considered. In males, if proteinuria is associated with hypercalciuria and nephrocalcinosis, Dent disease, an X-linked proximal tubulopathy that eventually leads to end-stage renal disease, should be considered, and the urine should be tested for 2microblobulin. Significant proteinuria with edema suggests nephrotic syndrome, which in most children suggests minimal change nephrotic syndrome. An age younger than 1 year or older than 10 years plus significant hematuria, azotemia, and hypertension are red flags that suggests a cause of nephrosis other than the more benign minimal change disease. Fever and abdominal pain in a patient with nephrotic syndrome should suggest spontaneous primary bacterial peritonitis. Changing patterns in the histopathology of idiopathic nephrotic syndrome in children. Plasmapheresis treatment for recurrent focal sclerosis in pediatric renal allografts. The prevalence of heavy proteinuria and progression risk factors in children undergoing urinary screening. Nephrotic syndrome in children: Prediction of histopathology from clinical and laboratory characteristics at time of diagnosis. The primary nephrotic syndrome in children: Identification of patients with minimal change nephrotic syndrome from initial response to prednisone. Genetic causes of focal segmental glomerulosclerosis: implications for clinical practice. Pan Hematuria is a common issue faced by primary physicians who care for children. While it can cause great anxiety in the patient and family when it presents as gross hematuria, rarely does hematuria alone herald a serious illness during childhood. Indeed, despite thorough evaluation, no cause can be found in a large percentage of children who have hematuria. Nearly 40% of children who present with gross hematuria and 80% of patients with persistent, isolated microscopic hematuria have no identifiable cause despite a thorough investigation. This raises the question of how much investigation should be performed on a child who presents with hematuria, particularly if it is isolated microscopic hematuria because the evaluation can be costly and at times invasive. Those children who present with gross hematuria or microscopic hematuria with associated signs or symptoms deserve a thorough evaluation. These two groups contain those more likely to have an identifiable cause and include the subset that has an acute or potentially serious illness that can progress to significant morbidity or sequelae if not identified and treated. Associated symptoms and signs that indicate the need for prompt evaluation include other urinary or systemic symptoms that led to testing the urine for blood, and findings of hypertension, edema, poor growth, fever, or other systemic signs at presentation. The more difficult question is how much testing is required of an apparently healthy child discovered to have isolated microscopic hematuria on routine screening urinalysis. Thorough testing of such a child with no symptoms, a normal physical examination, and no significant family history of kidney disease rarely identifies a cause of hematuria. Therefore, the utility of performing a screening urinalysis in children, with the potential attendant costly and usually uninformative additional investigation, has long been questioned. The American Academy of Pediatrics does not recommend screening urinalysis for early school-aged children. It is reasonable to screen children who have a significant family history of kidney disease, particularly if there is a family history of hereditary nephritis. If no hemoglobin is found on macroscopic urinalysis, then causes of urine discoloration other than hematuria need to be considered (Table 20. One fairly common presentation that can be particularly frightening to a parent is finding a pink or red-tinged wet diaper, thought to be blood in the urine. This most often is from a simple benign entity commonly called red diaper syndrome, caused by precipitation of urate crystals in the diaper. A macroscopic urinalysis negative for heme indicates this to be the most likely cause, and in an otherwise healthy infant, no further investigation is warranted. If red blood cells are found in the urine of a child with a history suggestive of gross hematuria, then evaluation for potential causes is needed (Tables 20. History Development of pain with the onset of hematuria usually indicates a lower urinary tract source. Irritative symptoms, such as dysuria, urgency, or frequency can be seen in bleeding from the bladder from a variety of causes. Severe and episodic or colicky flank or abdominal pain should raise suspicion for urolithiasis, which may have accompanying dysuria as the stone is being passed. Urinary tract obstruction, such as posterior urethral valves in boys or ureteropelvic junction obstruction in either sex, may remain occult until infection or trauma causes hematuria. In the former, the only preceding symptoms may be a boy who voids only infrequently, commonly strains to void, or has ongoing urinary incontinence beyond the toddler years. Bleeding from renal tumors is an uncommon cause of gross hematuria in children, but should be considered particularly in the setting of associated abdominal pain, a palpable mass, or passing of blood clots. Gross hematuria due to glomerular disease is rarely accompanied by significant pain, though some may report mild abdominal pain or flank discomfort. Clues to underlying glomerular disease may be a recent history of pharyngitis, streptococcal skin infection, or other febrile illnesses, indicating possible acute postinfectious glomerulonephritis. Patients with glomerulonephritis or renal insufficiency may report shortness of breath, edema, or weight gain from fluid retention. Carefully defining the appearance of the urine can be the first and a major clue to the origin of the blood. Hematuria emanating from a nonglomerular, lower urinary tract source can present as frankly bloody urine varying in color from dark red, cherry, or pink-tinged urine. Blood seen at the urethral meatus or only on initiation of voiding suggests a urethral source. Patients with African ancestry should be queried for personal or family history of sickle cell hemoglobinopathy, since gross hematuria from renal papillary necrosis can occur in those with sickle cell disease as well as in children with simple sickle cell trait. Medication history can uncover a cause of gross hematuria from drug-induced interstitial nephritis, seen with several antibiotics, anticonvulsants, or nonsteroidal antiinflammatory drugs, the latter of which can also cause papillary necrosis. Cyclophosphamide can cause a severe hemorrhagic cystitis, which usually has concomitant prominent bladder symptoms. A history of frequent or severe bleeding from other sites, such as heavy menses, prolonged nosebleeds, hemarthroses, or significant bleeding associated with surgical procedures suggests an undiagnosed bleeding disorder. Exposure history to tuberculosis should be obtained, as well as a travel history, as parasitic infections such as schistosomiasis of the bladder, uncommon in Western societies, is common in other parts of the world. Questions specific to other potential sources of blood in the urine include those directed at foreign body from selfinstrumentation of the urethra, trauma, sexual abuse, and menstruation. Extreme sports activities such as running a marathon or long distance cycling can cause gross hematuria. Review of the family history is important to uncover hereditary nephritis, hereditary cystic kidney disease, or potential benign familial hematuria. A family history of kidney disease leading to end-stage renal failure, especially if in men in multiple generations and if not clearly due to diabetes mellitus, would suggest Alport syndrome, the most common cause of hereditary nephritis. Alport syndrome is an X-linked recessive disorder that may cause gross hematuria in childhood although more often it is microscopic. When gross hematuria occurs in Alport syndrome, it is often triggered by any infectious process such as a common cold. The gross hematuria then subsequently clears, but microscopic hematuria is a persistent finding. The early clinical features of hereditary nephritis can be exactly the same as benign familial hematuria, but then evolve to develop other features. Early in the course of the disease, there is no associated proteinuria, but that feature develops later, often in childhood as the nephritis progresses. Hearing loss is a common but variable feature of Alport syndrome that tends to run in affected families. Female family members who are carriers usually have persistent and isolated hematuria that does not progress, but on occasion may develop progressive nephritis. Recurrent, painless gross hematuria is often seen in young patients with IgA nephropathy in association with concurrent respiratory illness. Recurrent fever, weight loss, alopecia, mouth ulcers, chest pain, fatigue, and arthritis suggest systemic lupus erthythematosis. The primary difference in family history that separates benign familial hematuria from progressive hereditary nephritis is that members of sequential generations of the family with benign familial hematuria, either male or female, have persistent isolated hematuria that never progresses to significant renal disease. The genetics of benign familial hematuria due to thin basement membrane nephropathy has been defined and includes mutations that are identical to those seen in some patients with autosomal recessive forms of progressive hereditary nephritis. Patients with thin basement membrane nephropathy, or benign familial hematuria, may be carriers of genes that cause autosomal recessive Alport syndrome. Kidney stone disease can be familial and in some cases related to specific genes, as in X-linked recessive nephrolithiasis (Dent disease) or primary hyperoxaluria. Therefore, family history of earlyonset nephrolithiasis, especially in siblings, should be sought in children presenting with gross hematuria and symptoms or imaging that indicate kidney stone disease as the cause. A family history of a bleeding disorder such as hemophilia or platelet disorders should be sought. Physical Examination the initial focus of the physical examination should be for evidence of systemic disease for which the hematuria is one manifestation, and for potential sequelae of renal disease. Accurate measurement and attention to blood pressure, recognizing age differences in blood pressure, is critical. Hypertension may be the sole feature on physical examination that indicates underlying acute glomerulonephritis, or chronic kidney disease from several causes. The finding of edema in this context is highly suggestive of underlying renal parenchymal disease, either acute or chronic, with likely accompanying renal insufficiency. Examination of the abdomen may reveal abdominal or flank masses that could be tumors, cystic kidneys, or urinary obstruction. The most common renal tumor in childhood, typically seen in young children (ages 1-4 years), is Wilms tumor, though other types occur. Suprapubic tenderness may indicate bladder infection, stone, or other less common causes of bladder pathology as the source of blood. The genitalia may need to be inspected for blood at the urethral meatus that suggests a urethral source, tears or lacerations due to abuse or accidents such as from straddle injuries, or to look for a foreign body. Laboratory Tests Macroscopic and microscopic examination of the urine is the first essential step in laboratory evaluation. If no heme is found on macroscopic examination, then other causes of urine discoloration need to be considered (see Table 20. If urine is heme positive but no red cells are seen, and there is no evidence for rhabdomyolysis or acute hemolytic disease, then other reasons for the findings need to be considered. Urine test strips can on occasion be falsely positive for blood if the urine is infected with peroxidaseproducing bacteria.

In some highly motivated and successful children anxiety ulcer order venlor without a prescription, the headaches may be a reaction to the stress associated with achievement anxiety nightmares buy cheap venlor 75mg online. In this instance anxiety breathing gif purchase venlor 75mg, school attendance is usually perfect and the patient continues to achieve in all realms anxiety symptoms keyed up purchase venlor 75 mg overnight delivery. Patients with tension-type headaches have normal neurologic and physical findings anxiety symptoms high blood pressure 75mg venlor with mastercard, except for possible tenderness along the affected muscles anxiety disorders order venlor 75mg. Childhood migraines are similar to those in adults; however, several features distinguish migraine in children from adult migraine. In children, the headaches are less frequent, are shorter in duration, and respond better to treatment. Pain is more frequently bilateral in children, though tends to become unilateral after the onset of puberty. Prevalence is higher in boys prior to puberty, though prevalence is higher in girls following the onset of puberty. A family history of migraines is common, with up to 90% of children having a 1st- or 2nd-degree relative with recurrent headaches. Migraine and migraine variants occur in early childhood but with an unknown prevalence, as diagnostic criteria for migraine are often insufficient in young children and infants, in whom the headaches tend to be shorter or have less typical features. While the diagnosis of migraine is typically made later in childhood, a careful retrospective history of infancy and early childhood events may reveal early episodic symptoms consistent with migraine, including pallor, vomiting, photophobia, phonophobia, fussiness, and sleepiness occurring outside the context of concurrent illnesses. Furthermore, benign paroxysmal torticollis, cyclic vomiting syndrome, and benign paroxysmal vertigo are episodic syndromes that may be associated with the diagnosis of migraines later in life. There is often no temporal pattern, although in postmenarchal females, migraines may cluster around particular phases of the menstrual cycle. Unless the migraines tend to cluster, patients rarely have migraines more than twice a week. The most common migraine precipitants are specific foods and food additives, such as chocolate, hard cheeses, onions, yeast, and beans. Other precipitants include menstruation, caffeine withdrawal, hunger, estrogen exposure (typically via oral contraceptives), sleep deprivation, stress, heat, and exertion. Migraine without aura is the most common migraine phenotype in pediatric patients. Criteria assist in the diagnosis of migraine without aura and are based on the number and duration of episodes, as well as symptoms and associated findings (Table 28. It has been recognized that children may have shorter-duration headaches, so an allowance has been made to reduce the duration to 2-72 hours or 1-72 hours with diary confirmation. At times, though, the pain of an episode may be sudden and severe, prompting concern for a thunderclap headache. More typically, pain increases in severity over the course of an individual episode and becomes throbbing. Because most patients are sensitive to motion, light, and noise during a migraine attack, they search for a dark and quiet place to sleep. Aura consisting of visual, sensory, and/or speech/language symptoms, each fully reversible, but no motor, brainstem, or retinal symptoms C. In migraine with aura, the headache is preceded by sensory signs or symptoms termed an aura, which is caused by vasoconstriction and diminished blood flow to the affected region of the brain. Sensory auras are less common than visual auras and may consist of numbness or tingling. Diplopia, vertigo, and vomiting should prompt evaluation for a posterior fossa abnormality, such as a mass or a vascular malformation. Hemiplegic migraine has an aura that consists of unilateral motor weakness and visual, sensory, and/or speech/language symptoms that are fully reversible. Aura consisting of visual, sensory, and/or speech/language symptoms, each fully reversible, but no motor or retinal symptoms C. At least 1 aura symptom spreads gradually over 5 or more min, and/ or 2 or more symptoms occur in succession 2. Severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15-180 min (when untreated)* C. At least 1 of the following symptoms or signs, ipsilateral to the headache: a) Conjunctival injection and/or lacrimation b) Nasal congestion and/or rhinorrhea c) Eyelid edema d) Forehead and facial sweating e) Forehead and facial flushing f) Sensation of fullness in the ear g) Miosis and/or ptosis 2. Attacks have a frequency between 1 every other day and 8 per day for more than half of the time when the disorder is active E. This migraine subtype is extremely rare, and other causes of the vision disturbance should be investigated prior to designating this diagnosis. The childhood periodic syndromes, or episodic syndromes that may be associated with migraine, are a group of potentially related symptoms that occur with increased frequency in children with migraine. Some of these have included gastrointestinalrelated symptoms (motion sickness, recurrent abdominal pain, recurrent vomiting including cyclic vomiting, and abdominal migraine), sleep disorders (sleepwalking, sleeptalking, and night terrors), unexplained recurrent fevers, and even seizures. Confusional migraine and Alice in Wonderland syndrome are rare migraine with aura variants that occur primarily in children. Confusional migraine begins after 5 years of age and usually converts to typical migraine as the patient gets older. Episodes begin with an alteration in consciousness, which may include varying degrees of lethargy, agitation, and stupor. The aura of Alice in Wonderland syndrome is characterized by perceptual disturbances in which the sense of proportion or distance, particularly with respect to the body, is distorted. Patients with migraine may have neurologic deficits that persist during and after the headache. These deficits include hemisensory symptoms, hemiparesis, aphasia, visual loss, and alteration in consciousness. These symptoms usually last for the duration of the headache but may remain for days following headache abatement. Permanent neurologic deficits are rare but may occur if the vasoconstriction is severe and causes infarction. This prolonged headache is usually associated with protracted vomiting and dehydration. Some disorders that feature migraine with aura episodes have an identified genetic etiology. This diagnosis must be considered in children with coexisting epilepsy, mental retardation or regression, and myopathy. Cluster headaches are characterized by episodes of pain interspersed between long periods of remission (Table 28. Pain is unilateral and localized to the eye and temple but may spread to other parts of the head. Lacrimation, rhinorrhea, sweating, and nasal stuffiness usually accompany the headache. Patients find it impossible to rest, and they become agitated and restless during an attack. This is in sharp contrast to a migraine, in which the patient is quiet and withdraws to a dark cool room for sleep. Episodic cluster headaches occur in a series that may last for weeks or months, separated by remission periods of months to years, whereas chronic cluster headaches are defined as occurring for more than 1 year without such a remission period, or with remission periods that last less than 1 month. Aneurysms and Arteriovenous Malformations Arterial aneurysms may be congenital (berry) or caused by an infectious process (mycotic). The pain is acute in onset and associated with nuchal rigidity, emesis, and changes in sensorium. In half of the cases, patients report having previous headaches before having the headache associated with the rupture. If the clinician suspects a leaking or ruptured aneurysm, rapid neurologic and neurosurgical care is mandatory. Paroxysmal Hemicrania Paroxysmal hemicrania is characterized by shorter attacks (2-30 minutes) and absolute prevention with and response to indomethacin. Chronic paroxysmal hemicrania consists of frequent and intense unilateral headaches. Although it usually begins in adulthood, chronic paroxysmal hemicrania may affect older children and adolescents. Patients have at least 20 attacks a day, and the pain may awaken the patient from sleep. Because the symptoms of chronic paroxysmal hemicrania are similar to those of vascular malformations of the brain, a neuroimaging study should be performed to rule out malformation before the diagnosis of chronic paroxysmal hemicrania is made. Secondary Headaches Arteritis, Cerebral Venous Thrombosis, and Vascular Dissection Vascular dissection may present with a headache that precedes ischemic symptom development by hours to days. These headaches are typically persistent, nonthrobbing, and unilateral but may be throbbing, thunderclap, and steadily worsening. Infection, coughing, vomiting, and connective tissue disorders such as Ehlers-Danlos disease are risk factors. The headache is generally constant and may have qualities of both chronic tension-type and migraine headaches. Other features of this syndrome are fatigue, dizziness, vertigo, poor memory, decreased reaction times, and inability to concentrate. About 70% of patients recover within a year, but 15% are still symptomatic after 3 years. Post-traumatic headache is considered acute if duration is less than 3 months and chronic if over 3 months. Even though postconcussive syndrome is more common in persons with a history of psychologic or psychosomatic illness, a neuroimaging study may be necessary to exclude the rare possibility of a chronic subdural hematoma. Vasculitis Vasculitis is an important cause of headaches in adults; however, in children, headache is rarely the presenting manifestation of this disorder and is instead a less frequent associated finding. Because of the increased risk of systemic hypertension in patients with vasculitis, it is important to include a blood pressure measurement as part of the complete history and physical examination. When systemic lupus erythematosus and mixed connective tissue disorders affect the central nervous system, children may present with seizures and mental status changes. More commonly experienced symptoms are focal neurologic deficits such as weakness of the limbs and face or speech abnormalities; as such, every child presenting with a focal neurologic deficit must undergo evaluation for stroke. If papilledema is present, neuroimaging should be obtained prior to lumbar puncture to evaluate for other causes of papilledema, such as a tumor or hydrocephalus (see Table 28. If the patient does not have a sixth cranial nerve palsy, then the diagnosis may be suggested (but not confirmed) if 3 of the following imaging requirements are met: empty sella, flattening of the posterior aspect of the globe, distention of the perioptic subarachnoid space with or without a tortuous optic nerve, and transverse venous sinus stenosis. Ongoing observation with recurrent exams, imaging, and studies is indicated to confirm the diagnosis. All patients with pseudotumor cerebri should be monitored closely with special attention to ocular findings, as they are at risk for development of permanent visual impairment. Headache in pseudotumor cerebri may be intermittent or constant and may resemble a migraine. Pseudotumor cerebri may be either primary or secondary to a variety of medical conditions. In idiopathic intracranial hypertension, a subset of primary pseudotumor cerebri, the typical patient is postpubertal, obese, and female. Pseudotumor cerebri may also be due to obstructive, toxic, metabolic, or hormonal causes that may often be revealed through a thorough history and physical examination (Table 28. In addition to headache and papilledema, signs and symptoms may include sixth and seventh cranial nerve palsies and visual field changes. In severe cases, the retinal blind spot may enlarge, and the visual fields may become constricted. Diagnosis in most cases is based on the historical presentation and the demonstration of an elevated cerebrospinal fluid opening pressure on a lumbar puncture obtained in the lateral position. Slowly developing hydrocephalus initially causes mild pain, whereas rapidly developing hydrocephalus causes severe pain. Most patients with hydrocephalus have morning headaches that lessen after they arise, though pain may also be constant. Physical examination reveals signs of increased intracranial pressure, such as papilledema or tenderness of the neck. Macrocephaly is present in young children with unfused cranial sutures and in those with long-standing hydrocephalus. The head growth chart is especially important in the evaluation of children with hydrocephalus. Head growth is abnormal if the plot of sequential head circumferences crosses percentile lines. The pain is maximum and severe at the onset of the activity and then resolves in seconds. Cough headaches, which are much shorter than are exercise-induced vascular headaches, may be caused by both benign and life-threatening conditions. Structural causes of cough headache include brain tumors, cysts, and Chiari malformations. The results of the physical examination are usually normal, even when structural lesions cause this syndrome. The etiology of the headache is due to traction on the dura and vessels at the base of the brain. The headache associated with intracranial hypotension typically improves while the patient is recumbent and worsens upon sitting or standing. The most common cause of a headache from intracranial hypotension is a persistent cerebrospinal fluid leak following lumbar puncture. Patients describe a severe headache within seconds after assuming an upright position. Intracranial Masses Brain neoplasms are the second most common type of childhood malignancy, though the overall incidence is low. Headaches caused by hydrocephalus may develop rapidly, whereas traction on dural or vascular structures from tumor growth causes a slow and progressive headache.

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Diseases

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• Charcot Marie Tooth disease type 1B
• Asbestosis
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• Cogan syndrome
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