4. PARTICIONES INTERIORES
4.3. DB-SE: Exigencias básicas de seguridad estructural
• Psychological approaches are the treatment of choice because they are more effective in the short term, probably also in the long term, but hourly sessions of specialist therapy may be needed.
• The effective components include the following:
Educational: nutritional, weight control.
Behavioral: food and purging diary, prescription of regular meals, stimulus control to limit meal size, distraction or relaxation to interrupt symptomatic behaviour.
Cognitive: modification of distorted beliefs about shape and weight, strengthening of coping resources, stress management, problem solving, communication and assertiveness skills.
Treatment aims
To restore normal eating patterns.
To provide psychologic support and treatment.
To reach an early diagnosis, which leads to better outcome.
Prognosis
• 50%–60% of patients are asymptomatic after treatment. 40% have ongoing prob-lems.
• Relapse is common in the first year after treatment.
• After 5 y, one third recover, one third have some symptoms, and one third are still affected.
• Self-harm is common in the 30% of patients with borderline personality dis-orders (ie, ~30% of these or ~10%–20%
of all patients).
• Mortality rate is 5%–18%.
Follow-up and management
• 6-monthly follow-up is needed.
Key references
1. Kreipe RE: Eating disorders among children adn adolescents. Pediatr Rev 1995, 16:
370–379.
2. Ratnasuriya RH, Eisler I, Szwukler GI, et al.
Anorexia nervosa: outcome and prognostic factors after 20 years. Br J Psychiatry 1991, 158: 495–502.
3. Fisher M, Golden NH, Kutzman DK, et al.
Eating disorders in adolescents: a review.
1995, 16: 420–437.
Encephalitis
Diagnosis
Symptoms
Headache, altered mental status (delirium, lethargy, confusion), behavioral abnormality: may progress to obtundation, coma.
Speech disturbance, limb weakness, incoordination, involuntary movements:
indicating focal cerebral involvement.
Seizures.
Signs
Drowsiness, confusion, irritability, coma.
Nuchal rigidity due to associated meningeal inflammation (may be absent).
Fever (may be absent).
Associated focal neurological findings: eg, hemiparesis, dysphasia (especially in herpes simplex encephalitis).
Ataxia, nystagmus, myoclonus, involuntary movements, extensor plantar responses.
Cranial nerve palsies: due to associated meningeal involvement (infrequent).
Evidence of systemic involvement: eg, cutaneous lesions in some infants with neonatal herpes simplex encephalitis.
Investigations
Cranial CT or MRI: may help to exclude other causes and may show brain edema; focal inferior temporal and orbital frontal damage with herpes simplex may take several days to become apparent (especially on noncontrast CT).
Lumbar puncture for cerebrospinal fluid (CSF) analysis: CSF is occasionally normal, but may be under increased pressure and usually shows lymphocytic pleocytosis, modestly elevated protein, and normal glucose concentration.
Erythrocytes are sometimes present in necrotizing encephalitides (eg, due to herpes simplex). Enzyme-linked immunoassays for viral antigens and gene amplification with polymerase chain reaction are increasingly available to aid early specific diagnosis, but are not completely sensitive.
Specific viral antibody titers: showing a significant rise is helpful in retrospect.
Electroencephalography: typically shows widespread slow activity; periodic complexes or focal slowing over temporal region are particularly suggestive of herpes simplex encephalitis. Brain biopsy: is generally not necessary but is occasionally helpful when the diagnosis is in doubt (eg, to evaluate for tumor, parasitic or fungal infection, and so on).
Complications
Seizures and status epilepticus: often occur and require vigorous treatment.
Cerebral edema: may cause transtentorial herniation and calls for measures to reduce intracranial pressure.
Chronic neurologic residua: eg, mental retardation, motor or behavioral abnormalities, especially in necrotizing forms of encephalitis (eg, herpes simplex).
Differential diagnosis
Meningitis: bacterial, tuberculous, fungal, or viral.
Acute disseminated encephalomyelitis (may be triggered by preceding infection or vaccination, but is probably not caused by active infection of the brain).
Encephalopathy with systemic infection (eg, due to hyperpyrexia).
Metabolic encephalopathy: usually no fever, headache, or CSF abnormality.
Cerebral abscess, empyema, subdural hematoma, other mass lesions.
Neoplasm (eg, leukemia) with meningeal involvement.
Etiology
• Viral invasion of brain parenchyma causes an inflammatory reaction of vary-ing intensity, associated with perivascular cuffing with lymphocytes and other mononuclear cells and with destruction of nerve cells and glia; hemorrhagic necrosis may occur.
Epidemiology
• Herpes simplex virus (HSV) is the most common cause of sporadic encephalitis.
• Other herpes viruses, especially herpes zoster, cytomegalovirus, and Epstein-Barr virus, are common causes, particularly when immunity is impaired, as in trans-plant or AIDS patients.
• Arboviral encephalitides may occur in epidemics in which mosquitoes bite humans.
• Mumps encephalitis and subacute scle-rosing panencephalitis have declined in incidence with vaccination; the latter is a progressive late complication of measles infection.
• Progressive multifocal leukoen-cephalopathy is seen in immunosup-pressed patients and is caused by a human polyoma virus.
• HIV infection may cause meningoen-cephalitis at seroconversion and later, a slowly progressive dementia.
Encephalitis
Treatment
Diet and lifestyle
Not relevant.
Pharmacologic treatment
• No effective treatment is available for many of the viruses causing encephalitis; often, the specific causative virus is not identified.
• Seizures require anticonvulsant administration.
• Full supportive measures are necessary during what is often a self-limiting illness with good recovery.
• Ventilation, mannitol, and dexamethasone can be used acutely to manage edema.
• Intravenous acyclovir started early reduces the morbidity and mortality of herpes simplex encephalitis; treatment should not await the outcome of brain biopsy, which is seldom appropriate.
Standard dosage Acyclovir, 500 mg/m2every 8 h (children 12 mo of age or older); 10 mg/kg/d every 8 h (children 3–12 mo of age); 10–20 mg/kg every 8 h (for neonatal HSV in term infants). Duration is 14–21 d.
Contraindications Hypersensitivity.
Special points Renal impairment necessitates dose reduction.
Main drug interactions Possible interaction with zidovudine.
Ganciclovir may be of benefit when cytomegalovirus is the probable cause.
Main side effects Acyclovir: may cause transient elevation of serum BUN/creatinine.
Ganciclovir may cause granulocytopenia or thrombocy-topenia, requiring dosage reduction or discontinuation.
Prevention
• Infants with perinatal exposure to HSV require isolation if born vaginally or if the interval between rupture of membranes and delivery by caesarian section exceeds 4–6 hours. Close observation and regular cultures (every 24–48 hours, including urine, rectum, mouth, and nasopharynx) are indicated; for positive cultures, acyclovir should be administered. Prophylactic treatment with acyclovir should be considered if the maternal infection appears to be primary (ie, first episode).
• A mother with active herpes labialis (cold sores) or stomatitis should wear a disposable surgical mask when touching her newborn until the lesions are crusted and dried; direct contact (eg, kissing) is permissible only after the lesions are completely healed.
Treatment aims
To treat herpes simplex encephalitis early: this often implies presumptive treatment of patients with acyclovir if the etiologic agent is uncertain.
To prevent recurrent seizures.
To control raised intracranial pressure.
To provide optimal rehabilitation when necessary.
Prognosis
• The outcome varies with different causative viruses, the age of the patient, and associated underlying disease.
• Death and serious residual disability are frequent with herpes simplex when the diagnosis and treatment are delayed.
Follow-up and management
• Neurological rehabilitation is impor-tant for patients with residual disability.
• Rarely, relapses occur with herpes sim-plex encephalitis.
General references
Connelly BL, Stanberry LR: Herpes simplex virus infections in children. Curr Opin Pediatr 1995, 7:19–23.
O’Meara M, Ouvrier R:Viral encephalitis in children. Curr Opin Pediatr 1996, 6:11–15.
Encopresis
Diagnosis
Definition
• Encopresis (soiling) is a problem that has serious social implications for a child. The medical issues surrounding this problem are usually not complex but troubling to treat.
Symptoms
Repetitive fecal soiling that occurs without the control of the child: occuring after the child has become toilet trained, usually older than 4 years of age.
Other symptoms of note:whether the child perceives the soiling in advance of it occurring; the pattern of defecation prior to the onset of soiling; the process of toilet training; any emotional or psychological traumas such as child sexual abuse or impending divorce of the parents.
• It is important to know the timing of the onset of the problem as well as its duration.
• Evaluate the impact of the soiling on the child as far as family relationships, peer interaction, and impact on school attendance.
• A complete dietary history is important because dietary manipulation will be needed in the treatment phase.
Signs
• Examine the child for the presence of retained fecal mass; on rectal examination, note the position of the stool.
• Check for signs of lower spinal cord problems in evaluating motor strength and sensation in the lower extremities; check for bladder function; inspect the lumbosacral area for dimples or tufts of hair.
• Also evaluate the child’s psychological status by looking for signs of depression, personality disorders, or other symptom complexes.
Investigations
Abdominal radiography: to document the extent and position of the retained stool.
Rectal manometrics, rectal biopsy, or studies of lower spinal cord function:
will depend on the findings of the signs and symptoms evaluation, eg, consti-pation since birth will prompt a workup to rule out Hirshsprung’s disease.
Complications
• The main complications to this disorder are fecal impaction causing bowel obstruction and toxic megacolon.
• Other complications are related to the severe psychological injury that may occur. It is also important not to overlook the other elements in the differential diagnosis as to do so would delay their proper treatment; this is particularly true for spinal cord tumors.
Differential diagnosis
• Most often the child with encopresis will have concomitant constipation.
• Other elements of the differential include spinal cord tumors, unrecognized Hirschsprung’s disease, pelvic mass, unrecognized meningomyelocele, or psy-chiatric disorder.
• Although there are several elements to the differential diagnosis, usually history and physical examination make clear that the most common scenario by far is that of constipation with overflow
“paradoxical” soiling.
Etiology
• The etiology of encopresis is probably multifactorial, including diet, toilet train-ing techniques, genetics, and other behavioral characteristics such as con-cern for cleanliness. Clearly the issue of bowel motility is an important one.
Those with naturally slow motility are probably more at risk.
Epidemiology
• About 1.5% of second-grade students may have this problem.
• Males are much more commonly affected (ratio, 6:1).
• The onset of the condition often begins at school age, when children do not wish to use public facilities and thus begin to withhold stool.
Other information
• Recent studies indicate that some chil-dren have a relative insensitivity to their rectal sphincter sensors. Some will con-tract their external sphincter while try-ing to defecate.Whether this is cause or effect has yet to be proven.
Encopresis
Treatment
General information
• Education of the child and family is very important, because this is a chronic condition that needs the full participation of the parents and child if the treatment is to be successful.
• Once the diagnosis of encopresis is made, there must be a long-term commitment made on the part of the physician and the family.
Disimpaction: treatment begins with removal of the large fecal mass from the rectum. This can be difficult and painful for the child. At times a child will need to be hospitalized for disimpaction.
Prevention of impaction reoccurence: this is accomplished by a combination of therapies: stool softeners and dietary and behavioral modifications.
Stool softener administration: may be of the fiber type or the lubricant (mineral oil). Mild stimulants may also be needed, such as senna or bisacodyl.
Dietary changes: include adding roughage and fiber to the diet and decreasing the amounts of refined sugar and dairy products. The child should be
encouraged to take more fluids through the day. When mineral oil is being used on a twice a day basis, a multivitamin should be given between the doses.
Behavioral therapy: is aimed at giving the child a time and place to have a regular bowel movement at least twice each day. This is done by selecting a time after a meal and encouraging the child to sit on the toilet, with feet firmly planted, for 15 minutes by a timer, and allowing the bowel movement to occur.
Promotility agents: eg, cisapride; some success has been observed in children with chronic constipation.
Treatment aims
To educate the child and family.
To remove impaction.
To keep bowel movements soft while bowel wall tone is reestablished.
To teach child ways to maintain normal bowel patterns for the future.
To remediate any psychological injury.
Prognosis
• Almost 65%–75% will have a lasting improvement in the first 6 mo of treatment.
• For the 25% with continued problems, further investigation may be needed.
Patient may also benefit from more intensive psychotherapy or biofeedback techniques.
Follow-up and management
• Close and careful follow-up is very important.This is a chronic condition and, like asthma or diabetes, it must be followed closely and progress moni-tored. Often after an initial period of success there may be reversal to old habits.There may be need for the child and family to keep a careful diary of intake and toilet habits. A 6-mo period of therapy is often the least possible in order to be successful.
Other information
• In this condition, parent and patient support groups are both educational and decrease the amount of social isolation and stigma that the patients feel.
• For difficult, seemingly intractable cases, specialty services are available at most large children’s centers.
General references
Hatch TT: Encopresis and constipation in chil-dren. Pediatr Clin North Am 1988, 35:257–280.
Nolan T, Oberklaid F: New concepts in the management of encopresis. Pediatr Rev 1993, 14:447–451.
Levine MD: Encopresis: its potentiation, evalua-tion, and alleviation. Pediatr Clin North Am 1982, 29:315–330.
Endocarditis
Diagnosis
Symptoms
Fever and sweating.
Easy fatiguability, malaise.
Palpitations.
Weight loss and anorexia.
Signs
Fever.
Tachycardia with new (or changing) cardiac murmur(s).
Splenomegaly.
Janeway lesions, splinter hemorrhages, Osler nodes, Roth spots: relatively rare in children.
Embolic phenomena: microscopic to kidney, results in hematuria); macroscopic, may cause vascular occlusion (GI, limbs), stroke, mycotic aneurysm, pulmonary embolism.