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A. Kasim, M.B.A., M.B.B.S., M.H.S.

Deputy Director, Loma Linda University School of Medicine

Structural Lesions That Cause Altered Consciousness in Humans To produce stupor or coma in humans, a disorder must damage or depress the function of either extensive areas of both cerebral hemispheres or the ascending arousal system, including the paramedian region of the upper brainstem or the diencephalon on both sides of the brain. Conversely, unilateral hemispheric lesions, or lesions of the brainstem at the level of the midpons or below, do not cause coma. Lesions of the brainstem may be very large without causing coma if they do not involve the ascending arousal system bilaterally. Even if blood flow or oxygenation is restored after 5 or more minutes, there may be widespread cortical injury and neuronal loss even in the absence of frank infarction. Alternatively, in some patients with less extreme cortical hypoxia, there may be a lucid interval in which the patient appears to recover, followed by a subsequent deterioration. Such a patient is described in the historical vignette on this and the following page. Fortunately, most such cases included pathologic assessment, which is also all too infrequent in modern cases. A companion already had died, apparently the result of an attempted double suicide. The neurologic examination was normal, and an evaluation by a psychiatrist revealed a clear sensorium with ``no evidence of organic brain damage. At home he remained well for 2 days but then became quiet, speaking only when spoken to . Hypoxia typically causes more severe damage to large pyramidal cells in the cerebral cortex and hippocampus compared to surrounding structures. The next day (13 days after the anoxia) he became incontinent and unable to walk, swallow, or chew. He was admitted to a private psychiatric hospital with the diagnosis of depression. Deterioration continued, and 28 days after the initial anoxia he was readmitted to the hospital. His blood pressure was 170/100 mm Hg, pulse 100, respirations 24, and temperature 1018F. His extremities were flexed and rigid, his deep tendon reflexes were hyperactive, and his plantar responses extensor. Histologically, neurons in the motor cortex, hippocampus, cerebellum, and occipital lobes appeared generally well preserved, although a few sections showed minimal cytodegenerative changes and reduction of neurons. Pathologic changes were not present in blood vessels, nor was there any interstitial edema. The striking alteration was diffuse demyelination involving all lobes of the cerebral hemispheres and sparing only the arcuate fibers (the immediately subcortical portion of the cerebral white matter). The condition of delayed postanoxic cerebral demyelination observed in this patient is discussed at greater length in Chapter 5. A series of drawings illustrating levels through the brainstem at which lesions caused impairment of consciousness. For each case, the extent of the injury at each level was plotted, and the colors indicate the number of cases that involved injury to that area. The overlay illustrates the importance of damage to the dorsolateral pontine tegmentum or the paramedian midbrain in causing coma. As a result, it is no exaggeration to say that virtually any deficit due to injury of a discrete cortical area can be mimicked by injury to its thalamic relay nucleus. Hence, thalamic lesions that are sufficiently extensive can produce the same result as bilateral cortical injury. The most common cause of such lesions is the ``tip of the basilar' syndrome, in which vascular occlusion of the perforating arteries that arise from the basilar apex or the first segment of the posterior cerebral arteries can produce bilateral thalamic infarction. Other causes of primarily thalamic damage include thalamic hemorrhage, local infiltrating tumors, and rare cases of diencephalic inflammatory lesions. Examination of her brain at the time of death disclosed unexpectedly widespread thalamic neuronal loss. However, there was also extensive damage to other brain areas, including the cerebral cortex, so that the thalamic damage alone may not have caused the clinical loss of consciousness. On the other hand, thalamic injury is frequently found in patients with brain injuries who eventually enter a persistent vegetative state (Chapter 9).

Syndromes

• You have weakness or are unable to move (paralysis), along with numbness or tingling
• Breathing difficulty
• Monitoring symptoms that might suggest the disease is getting worse, such as fatigue, weight loss, increased pain, decreased bowel and bladder function, and weakness
• Complete blood count (CBC)
• Spastic arterial disease (arterial contractions brought on by cold or emotion)
• High erythrocyte sedimentation rate (ESR)
• Ductal carcinoma starts in the tubes (ducts) that move milk from the breast to the nipple. Most breast cancers are of this type.
• Urinalysis
• Dementia develops or a sudden change in mental status occurs

Her blood pressure and heart rate are normal for her age and body mass index is at the 80th percentile. Symptoms of imperforate hymen include lack of menses, cyclical abdominal or back pain, urinary retention, constipation, and lower extremity edema. On physical examination, an abdominal mass can be palpated, as well as a bluish bulging mass at the introitus from accumulation of menstrual bleeding. Treatment of an imperforate hymen requires a hymenotomy, a surgical resection of the membrane. However, a low transverse vaginal septum can be distinguished from an imperforate hymen with the Valsalva maneuver. During the Valsalva maneuver, bulging is seen with an imperforate hymen, and not with a low transverse vaginal septum. Vaginal agenesis is typically characterized by absence of the proximal vagina and absence or hypoplasia of the uterus. In addition to those findings, ultrasonography may reveal additional abnormalities such as urinary tract anomalies. Uterine duplication anomalies are often asymptomatic unless an obstruction is present. Labial adhesions occur typically in the prepubescent population before the production of endogenous estrogen, which starts at puberty. Her physical examination is remarkable only for several papules located in the left antecubital fossa (Item Q23). It is especially prevalent in children who have atopic dermatitis, with a disrupted skin barrier and impaired cutaneous immunity. Papules vary in number and range in size from 1 to 6 mm in diameter, and can affect most body surfaces, although involvement of the palms, soles, and mucous membranes is rare. It is not known whether this represents a host response to the virus or underlying atopic dermatitis. Molluscum contagiosum is self-limited, therefore no intervention would be a reasonable choice for children who have only a few asymptomatic lesions. Especially in young children who do not tolerate discomfort well, cantharidin (a blister beetle extract) may be applied in the office to individual lesions. Alternative painless topical agents that may be applied at home include salicylic acid and a topical retinoid (eg, tretinoin or adapalene). For children who can tolerate discomfort, cryotherapy and curettage are effective. A less severe cardiovascular condition with a perfusing rhythm is not as likely because he is not breathing. Although a neurologic catastrophe (eg, trauma or spontaneous hemorrhage of a cerebrovascular malformation) should be considered as a possible cause of this event, it is significantly less likely without a supporting history. Appropriate life support responses for children include the algorithms of basic life support, in which it is assumed that there is only 1 responder, and pediatric advanced life support, which takes place in an environment in which many rescuers are involved and actions can be undertaken simultaneously. If no advanced airway, ie, an endotracheal tube or laryngeal mask airway, is present, a 15:2 compression-ventilation ratio should be followed. If an advanced airway is in place, 8 to 10 breaths per minute should be given with continuous chest compressions. Because the boy in the vignette presented with collapse and apnea, he is unlikely to have a perfusing rhythm. Palpation for a pulse in this setting may not be accurate, and could lead to a delay in definitive care. The cause of his collapse is likely cardiac, therefore jaw-thrust or chin-lift maneuvers would not be helpful. The precordial thump is no longer recommended in the latest American Heart Association guidelines. In the absence of trauma, immobilization of the cervical spine is not recommended. Part 15: neonatal resuscitation-2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. On physical examination, he is irritable and has a faint erythematous maculopapular rash principally over the lower extremities. While arboviral infections, including West Nile virus, can present with a nonspecific febrile illness or aseptic meningitis, they are a less common etiology in this age group, as they would require contact with the respective vector.

Allowing catch-up sleep on weekends can actually worsen delayed sleep phase syndrome and thus is discouraged. Appropriate physical activity should be encouraged for all children and exertion during the afternoon is unlikely to affect his sleep. Upon review of his social history, you discover that his grades have dropped significantly over the last year. He states that he drinks alcohol and smokes marijuana when alone and to feel better about life. His friends have told him to stop using marijuana because he forgets things when he is using it. All adolescents are then asked about whether they have ever ridden in a Car with a driver who has been drinking or using drugs, or whether they operated a Car while under the influence. Substance use screening, brief intervention, and referral to treatment for pediatricians. He is chronically infected with Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus. He does not have pulmonary hypertension and has not required chronic supplemental oxygen. Eight months ago, he was admitted to the intensive care unit when he required noninvasive respiratory support with bi-level positive pressure ventilation during a pulmonary exacerbation. In the United States, more than 50,000 children die each year, and a significant number of these deaths are attributable to a chronic medical condition. Medical and surgical treatment options have continued to evolve and have resulted in an increased life expectancy for many diseases that previously were associated with death during childhood. However, many illnesses are still associated with considerable morbidity and mortality. As such, all pediatricians should be educated in the development and implementation of care directives; patients and their families should be engaged in the development of these plans and the plans should be updated as needed and as the course of the disease changes. While many pediatric patients with chronic illnesses are under the care of a subspecialist, the development of an advanced directive is not the sole responsibility of the subspecialty physician. Families benefit if the care team (including the general pediatrician) is coordinated in their approach to these discussions. In contrast, no similar legislation has been directed at children and adolescents. It is generally appreciated that end-oflife discussions allow patients and families to examine their disease and their treatment preferences. When inquiries are made as to end-of-life preferences, literature has shown that the majority of families choose home or hospice as a preferred location of death for their child. In instances where care directives are not obtained, children are more likely to expire in the hospital. The intent of these discussions should not be interpreted as the health care team "giving up. In clinical research studies, the "assent" of younger children is routinely sought. The community of pediatric care providers will continue to benefit from a standardized approach to planning for end-of-life care. A longitudinal, randomized, controlled trial of advance care planning for teens with cancer: anxiety, depression, quality of life, advance directives, spirituality. The baby was born at term, by normal spontaneous vaginal delivery, after spontaneous rupture of membranes with clear amniotic fluid. The newborn took 20 mL of formula within 1 hour of birth, but has taken less with each subsequent feed. Her lungs are clear to auscultation bilaterally and her heart has a regular rate and rhythm. This is most likely caused by an inborn error of metabolism, and the test most likely to reveal the diagnosis is urine organic acids.

In any age group, the differential diagnosis includes adhesive capsulitis, calcific tendonitis, and a variety of other less common shoulder problems (avascular necrosis, scapulothoracic dysfunction, and infection). The Y-outlet view shows the acromial morphology with potential narrowing of the subacromial space. Initial Treatment the goal of treatment is to return the patient to painfree activity. If the pain is significant, an oral antiinflammatory medication can be prescribed. Once the painful period subsides, the patient may benefit from a course of physical therapy to strengthen the rotator cuff and scapular stabilizers. A subacromial corticosteroid injection can be considered in a patient who fails to respond to the initial treatment over 2 to 3 months. Patients who fail to respond to nonoperative management over 3 to 6 months may benefit from surgical treatment. This procedure involves removing the inflamed subacromial bursa and shaving the undersurface of the acromion (acromioplasty) to create more room in the subacromial space for the rotator cuff. There are a variety of options for patients with irreparable tears, including arthroscopic debridement, partial tendon repair, and tendon transfers. If biceps tendon pathology is found at the time of surgery, either tenodesis or tenolysis can be performed. Restoration of strength and function is the goal of subsequent postoperative therapy. Failure of the patient to adhere to postoperative physical therapy can result in a poor outcome. Osteoarthritis Degenerative or osteoarthritis occurs in the glenohumeral joint but is less common than in the hip or knee joints. Osteoarthritis of the glenohumeral joint has the same pathophysiology as in other joints with progressive articular cartilage destruction. History Patients with early osteoarthritis may have a clinical syndrome that is virtually indistinguishable from impingement syndrome. In patients with advanced osteoarthritis, pain is more likely to be chronic, occur at rest, and be resistant to standard analgesics and antiinflammatory medications. In general, active motion is decreased in all planes but loss of external rotation is often the most dramatic. Differential Diagnosis Adhesive capsulitis and inflammatory arthropathy can have similar presentations. The examiner must have a high index of suspicion for locked posterior shoulder dislocations in older patients who are poor historians as a result of dementia or stroke. Physical therapy for stretching and maintenance of motion is an important component of nonoperative treatment. Corticosteroid injections provide inconsistent and incomplete pain relief in this setting. Patients with concentric wear with or without some joint space preservation and reasonable motion may benefit from arthroscopic debridement. The goal of debridement is pain relief and postponement of prosthetic joint arthroplasty. The pegged glenoid component is cemented into the glenoid and is represented by the reproduction of the joint space. The central peg of the polyethylene glenoid component is identified by the horizontal radiopaque marker. Total shoulder arthroplasty introduces the risk of glenoid-sided prosthetic loosening and wear, which may require revision surgery. Miscellaneous Arthropathy A variety of other disease processes can lead to glenohumeral joint destruction. Inflammatory arthropathy such as rheumatoid arthritis can lead to joint destruction as a result of synovial disease. Although the clinical presentation may be similar to osteoarthritis with pain and loss of motion, there are some important differences. In particular, rheumatoid arthritis can result in rotator cuff deficiency and incompetence.