By D. Thorald. University of Delaware.

The thymus The thymus is a lymphoid organ found in the superior aspect of the anterior mediastinum generic 20 mg tadacip with visa. It is prominent on the chest radiograph of an infant as a result of the thoracic cavity being relatively small; however normal variations in radiographic appearances are common (Figs 4 cheap 20mg tadacip overnight delivery. It grows during early childhood to reach a maximum at approximately 15 years of age after which it undergoes regression. It is intensely active during childhood, producing thymus lymphocytes which form part of the human leukocyte antigen mechanism by which the body establishes its system of immunity. The heart The heart is prominent on the chest radiograph of an infant as a result of it lying transversely and occupying approximately 40% of the thoracic cavity. Pathology of the chest and upper respiratory tract Paediatric respiratory disorders generally result in airway obstruction. Clinical symptoms are dependent upon whether the obstruction is extra-thoracic or intra- thoracic but may include stridor (a harsh sound usually heard on inspiration as a result of a partially obstructed extra-thoracic/upper airway), wheeze (an expi- ratory noise produced by partial obstruction of the intra-thoracic/lower airway), or crackles/rales (caused by fluid secretions within the alveolar spaces or ter- minal airways). The upper/extra-thoracic airway Adenoidal-tonsillar hypertrophy The adenoids (nasopharyngeal tonsils) are lymphoid tissue within the nasophar- ynx concerned with the protection of the upper airway. They are generally small at birth but steadily enlarge until approximately 8 years of age after which they normally regress. Children with hypertrophic (enlarged) adenoids may present clinically with mouth breathing, snoring or possible recurrent otitis The chest and upper respiratory tract 31 (a) (b) Fig. Clinically suspected adenoid hyper- 2 trophy can be confirmed on a lateral post-nasal space radiograph (Fig. Retropharyngeal abscess Retropharyngeal abscess is a rare condition presenting in infants (<1 year of age).

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Useful to confirm maturity of HO Prophylaxis ROM exercises Control of muscle tone Non Steroidal Anti-inflammatory Drugs (NSAIDs) Radiation—used perioperatively to inhibit HO in total hip replacement patients; concerns about ↑ risk of neoplasia limit its use in younger patient populations (e order tadacip 20mg fast delivery. Also 20mg tadacip visa, as radiation is used prophylactically to prevent HO formation of a particular joint, to use it in TBI patients would require essentially irradiation of the whole body (as HO can develop practically at any joint), which is not practical TRAUMATIC BRAIN INJURY 67 Treatment Diphosphonates and NSAIDs (particularly indomethacin) have been used on patients to arrest early HO and to prevent postop recurrence, but their efficacy has not been clearly proven (TBI population) ROM exercises—used prophylactically to prevent HO and also used as a treatment for developing HO (to prevent ankylosis) Surgery—surgical removal of HO indicated only if ↑ in function is a goal (to ↑ hygiene, sitting, etc. IVC filter used when anticoagulation is contraindicated Posttraumatic Epilepsy/Posttraumatic Seizures (PTS) Posttraumatic epilepsy is classified as: 1. Partial (simple, if consciousness is maintained, or complex, if not) The majority of PTS are of the partial type Posttraumatic seizures are further classified as: Immediate PTS—occur within the first 24 hours post injury Early PTS—occur within the first week (24 hours to 7 days) Late PTS—occur after the first week – Immediate PTS has better prognosis than early epilepsy; early PTS associated with increased risk of late PTS Incidence Varies greatly according to the severity of the injury, the time since the injury, and the pres- ence of risk factors (see below) 5% of hospitalized TBI patients (overall, closed-head injury) have late PTS 4%–5% of hospitalized TBI patients have one or more seizures in the first week after the injury (early PTS) (Rosenthal et al. A group of 4541 patients with TBI {characterized by loss of consciousness (LOC), posttraumatic amnesia (PTA), SDH or skull fracture}, were divided into three categories: Mild TBI—LOC or amnesia < 30 minutes Moderate TBI—LOC for 30 minutes to 24 hours or skull fractures Severe TBI—LOC or amnesia > 24 hours, SDH or brain contusion Incidence of seizures in the different categories: Mild TBI—1. There is no proof of change in outcome with prophy- lactic use of phenytoin (Temkin et al. TABLE 2–10 Anticonvulsant Medications: Uses and Adverse Reactions Medication Uses Adverse Reactions Carbamazepine Partial seizures Acute: stupor or coma, hyperirritability, Tonic-clonic; generalized convulsions, respiratory depression seizures Chronic: drowsiness, vertigo, ataxia, diplopia, Stabilization of agitation blurred vision, nausea, vomiting, aplastic anemia, and psychotic behavior agranulocytosis, hypersensitivity reactions Bipolar affective disorder (dermatitis, eosinophilia, splenomegaly, Neuralgia lymphadenopathy), transient mild leukopenia, transient thrombocytopenia, water retention with decreased serum osmolality and sodium, transient elevation of hepatic enzymes Gabapentin Partial seizures Somnolence, dizziness, ataxia, fatigue Lamotrigine Partial seizures Dizziness, ataxia, blurred or double vision, Tonic-clonic; generalized nausea, vomiting, rash, Stevens-Johnson seizures syndrome, disseminated intravascular coagulation Phenobarbital Partial seizures Sedation, irritability, and hyperactivity in Tonic-clonic; generalized children, agitation, confusion, rash, exfoliative seizures dermatitis, hypothrombinemia with hemorrhage in newborns whose mothers took phenobarbital, megaloblastic anemia, osteomalacia Nystagmus and ataxia at toxic doses Phenytoin Partial seizures Intravenous administration: cardiac Tonic-clonic; generalized arrhythmias, hypotension, CNS depression seizures Oral administration: disorders of the cerebellar Neuralgia and vestibular systems (such as nystagmus, ataxia, and vertigo), cerebellar atrophy, blurred vision, mydriasis, diplopia, ophthalmoplegia, behavioral changes (such as hyperactivity, confusion, dullness, drowsiness, and hallucination), increased seizure frequency, gastrointestinal symptoms, gingival hyperplasia, osteomalacia, megaloblastic anemia, hirsutism, transient liver enzyme elevation, decreased antidiuretic hormone secretion leading to hypernatremia, hyperglycemia, glycosuria, hypocalcemia, Stevens-Johnson syndrome, systemic lupus erythematosus, neutropenia, leukopenia, red cell aplasia, agranulocytosis, thrombocytopenia, lymphadenopathy, hypothrombinemia in newborns whose mothers received phenytoin, reactions indicative of drug allergy (skin, bone marrow, liver function) Valproic Acid Partial seizures Transient gastrointestinal symptoms such as Tonic-clonic; generalized anorexia, nausea, and vomiting; increased seizures appetite; sedation; ataxia; tremor; rash; alopecia; Myoclonic seizures hepatic enzyme elevation, fulminant hepatitis Absence seizures (rare, but fatal); acute pancreatitis; Stabilization of agitation hyperammoniemia and psychotic behavior From Rosenthal M, Griffith ER, Kreutzer JS, Pentland B. Rehabilitation of the Adult and Child with Traumatic Brain Injury 3rd ed. Their superiority over phenytoin has been debated (differences among these three agents are probably minimal); carbamazepine may be as sedating as phenytoin. Animal and clinical (extrapolated from strokes) studies suggest that phenytoin may impede recovery from brain injury (Dikmen, 1991) Second generation anticonvulsants, such as gabapentin and lamotrigine, may also be used for treatment of PTS as adjuvant agents (not approved yet for monotherapy). These agents appear to have fewer cognitive side effects, but are still under investigation in the TBI population. Anticonvulsant Medications: Common Drug Interactions Medication Drug Interaction Carbamazepine Increased metabolism of carbamazepine (decreased levels) with phenobarbital, phenytoin, and valproic acid Enhances metabolism of phenobarbital Enhances metabolism of primidone into phenobarbital Reduces concentration and effectiveness of haloperidol Carbamazepine metabolism inhibited by propoxyphene and erythromycin Lamotrigine When used concurrently with carbamazepine, may increase levels of 10,11 –epoxide (an active metabolic of carbamazepine) Half-life of lamotrigine is reduced to 15 hours when used concurrently with carbamazepine, phenobarbital, or primidone Reduces valproic acid concentration Phenobarbital Increased levels (as much as 40%) of phenobarbital when valproic acid administered concurrently Phenobarbital levels may be increased when concurrently administering phenytoin Phenobarbital has a variable reaction with phenytoin levels Phenytoin Phenytoin levels may increase with concurrent use of chloramphenicol, cimetidine, dicumarol, disulfiram, isoniazid, and sulfonamides Free phenytoin levels may increase with concurrent use of valproic acid and phenylbutazone Decreased total levels of phenytoin may occur with sulfisoxazole, salicylates, and tolbutamide Decreased phenytoin levels with concurrent use of carbamazepine Decreased carbamazepine levels with concurrent use of phenytoin Increased or decreased levels of phenytoin when concurrently administered with phenobarbital When concurrently used with theophylline, phenytoin levels may be lowered and theophylline metabolized more rapidly May decrease effectiveness of oral contraceptives Enhances metabolism of corticosteroids Valproic Acid Increases level of phenobarbital Inhibits metabolism of phenytoin Rare development of absence status epilepticus associated with concurrent use of clonazepam (Reprinted with permission from Rosenthal et al. It has been suggested to withdraw anticonvulsant medications after a seizure-free interval of 3 months to 6 months up to 1–2 years.

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