16_McClure_16.indd 591 11/14/2012 3:42:47 PM CHAPTER 16 Child and family psychiatry 592 Somatoform disorders and typical consultation \200\223liaison presentations This is a poorl y de \201 ned area with a whole host of overlapping terms, and confusions between descript ive terms and implied etiology. Some of the terms in common usage are: \200 Psychosomatic: include both illnesses brought on by stress, e.g. tension headache and physi cal symptoms secondary to psychiatric illness, e.g. hypothermia secondary to malnutrition i n anorexia nervosa. Somatoform are subdivided into: \200 \200 \200 \200 a very general and rather unhelpful term that can disorders: physical symptoms with no organic basis. These conversion disorders; chronic fatigue syndrome; pain syndromes, hypochondriasis; somatizati on disorder. Whilst many of these terms are entrenched, and so unlikely to disappear, the concept of som atoform disorders has been much criticized on the following grounds: \200 It implies a cause that is not demonstrable and often intuitively does not appear to be cor rect. It is often unacceptable to patients and parents and is therefore an obstacle to form ing a collaborative relationship. Its use may result in missing psychiatric or physical dia gnoses. There seems little relationship between this term and other diagnoses commonly appl ied to the same patients in non-mental health settings, e.g. irritable bowel, chronic fatig ue. \200 Conversion disorder See also b p.525. Conversion disorder is characterized by the presence of physical symptoms (e.g. paralysis, seizures, and sensory de \201 cits) or men- tal symp toms (e.g. amnesia), but without any evidence of physical cause. Previously called hysteria . Proposed underlying mechanism is transforma- tion of emotional con \202 ict into mental or physical symptoms. The postu- lated splitting off of mental processes from each other is referred to as dis- sociation. There may be secondary gain, e.g. when the child who is bei ng bullied at school develops paralysis, which keeps him at home. Conversion disorders are rare in childhood, particularly before the age of 8yrs. Treatment Principles of treatment include attempts to resolve any apparent emotion- al dif \201 culties, avoidance of unnecessary physical investigation, removal of secondary gain, and help in returning to normal life. Prognosis Generally favorable. Chronic fatigue syndrome See b pp.990 \200\223991 16_McClure_16.indd 592 11/14/2012 3:42:47 PM SOMATOFORM DISORDERS 593 Recurrent non-organic abdominal pain See also b pp.310, 991. The child \200\231s complaints of recurrent abdominal pain are not found to have a physical basis. \200 710 \200\22315% of children at some point, usually Common, affecting between 5 and 12yrs (n o apparent gender or social class bias). There may be associated symptoms of other pains, n ausea, or even vomiting. Pains are usually episodic and relapsing though may be more persis tent. An uncommon variant is the periodic syndrome where episodes of pain are associated wi th vomiting, headache, and low grade pyrexia. This is thought by some to be a form of migra ine. Differentiation from organic pathology may be dif \201 cult. Features that may help includ e the diffuseness of the pain, the tendency not to be woken by it, pains elsewhere in the b ody, anxiety, and depression in child and parent, and the lack of positive \201 ndings on physical examination. Treatment Generally a combination of reassurance, education about the links between stress and the body, psychological treatment where appropriate and avoidance of unnecessary physic al investigation and treatment. Prognosis Short-term outcome is usually favorable though it is not known whether this is du e to or in spite of treatment. In the longer term further episodes of non-organic pain are found in a large minority of cases. Selective eating This is a condition of younger children that in most, though not all, reso lves in the teenage years. These children eat only a limited range of foods. In severe case s the restriction may be to only 3 or 4 foods. It is surprising that most children seem to ingest all the required nutrients in their very limited diet. To treat, a mixture of reassu rance and encourage- ment seems to be the best approach. More active intervention is indica ted when the child is malnourished and usually entails a gradual hierarchical desensitizati on program. 16_McClure_16.indd 593 11/14/2012 3:42:47 PM CHAPTER 16 Child and family psychiatry 594 Anorexia nervosa Epidemiology Anorexia nervosa is the third commonest chronic illness in te enage girls. Prevalence in the Western world is 70.5%. Whilst varying with age, a sex ratio of 9:1 (girls:boys) is fairly typical. Pre-pubertal cases are rare, but do occur. Bulimia nervosa is generally of youth onset. Causes Often unclear in individual cases; however, genetic pre-disposition, a perfectionist personality, and low self-esteem seem to be implicated. Dissatisfaction with weight and sh ape is relatively common in children as young as 8yrs and is presumably a vulnerability fac tor. The pathway into anorexia nervosa is through weight loss, either due to a desire to lo se weight or for some other reason such as depression/anxiety or, some- times, viral illnes s. Diagnostic criteria \200 Dietary restriction (may be accompanied by vomiting, exercise, laxative abuse, or other wei ght control methods) leading to signi \201 cant and unhealthy self-induced weight loss (e. g. to less than 85% of expected body weight for height or age or a BMI < 17.5) or to stunti ng of expected growth. Intense fear of gaining weight even when severely underweight. Body image distortion with dread of fatness. Amenorrhoea (may be \200 \200 p or s). In younger teenagers anorexic thoughts may often be either absent or hidden, e.g. fear of b ecoming fat may be absent because they \200\230know \200\231 they can control their weight . Individuals who exhibit signi \201 cant weight-losing behaviors, not explained by depres sion, a speci \201 c phobia, or physical ill- ness, may be referred to as having an atypic al eating disorder. Treatment The evidence-base for treatment is small. Management of anorexia ner- vosa in chi ldren and young people requires a team effort and virtually all cases will require intensiv e treatment with more than one therapeutic mo- dality. The key to success in individual tre atment is the engagement with the therapist rather than the type of therapy provided. Invol vement of the family through family therapy seems to be important. Treatment is likely to be lengthy and to involve attention to anorexic behaviors, to recogn izing and not acting on anorexic thoughts and feel- ings, and to returning to aspects of no rmal function such as school and home life. It is far preferable to work collaboratively wi th the young per- son. At times compulsory treatment (requires use of the Mental Health Act ) may be needed. Clearly, correction of dangerous weight loss or its secondary complica- tions may be urgent . Patients who are unable or unwilling to manage ade- quate oral nutrition may need nasogas tric feeding. In any rapid refeeding plan the risks of refeeding syndrome (b p.322) should be remembered. 16_McClure_16.indd 594 11/14/2012 3:42:47 PM ANOREXIA NERVOSA 595 Prognosis Anorexia nervosa is a serious psychiatric disorder that carries a signi \201 - c ant risk of mortality as well as considerable morbidity. Although some cases of anorexia in children and young people are mild and resolve with- out intensive treatment programs, man y will go on into adult services with chronic eating problems. Whilst the quoted long term outcomes for anorexia generally accept that a third will recover full, a third will make a partial recovery and a third with have chronic symptoms, this is taking into account the li fetime course of the illness. The prognosis for teenagers is generally better than for adul ts with most making a full recovery. This can, however, take years, and an interim step may be to learn how to live with the illness rather than be controlled by it. The risks to physical long term health are greater without early atten- tion to malnutrition and long term problems include: \200 \200 \200 \200 growth retardation; delayed or arrested puberty; reduced bone density; higher likelihood of low birth weight baby. Risk factors for poorer outcome \200 \200 \200 \200 \200 \200 \200 late onset; excessive weight loss; vomiting and purging as part of the clinical picture; po or social adjustment; poor parental relationships; being male; chronic course of illness. 16_McClure_16.indd 595 11/14/2012 3:42:47 PM CHAPTER 16 Child and family psychiatry 596 Bulimia nervosa Epidemiology Bulimia nervosa is rare before the age of 13yrs. Although onse t of the disorder is generally in mid- to late teens, it is unusual to present for help bef ore early twenties. In teenagers, bulimia may occur alongside other externalizing teenage b ehaviors such as sexual promiscuity, drug taking drinking, and self-harming. 90% + of cases are female and is distributed right across the social classes. In adult women, the inciden ce is 1 \200\2231.5% and it is 2 \200\2233 times more common than anorexia nervosa in adole scents. Bulimia is associated with westernized lifestyle with a lower prevalence in develop ing countries and rural areas. There may, or may not be, a preced- ing history of anorexia nervosa. Causes Similar factors contribute to the etiology of bulimia nervosa as are found for anore xia nervosa. Additional risk factors include: \200 \200 \200 \200 \200 \200 adverse family life events; family history of obesity; parental substance misuse; family hi story of affective disorder; poor social network; critical parents. In contrast to anorexia nervosa, bulimia is associated with high expression of emotions, im pulsivity, and a chaotic lifestyle. Diagnostic features \200 Persistent preoccupation with eating. Craving for food with recurrent episodes of binge eat ing, associated with feeling out of control. Regular use of mechanisms to reduce weight gai n from binging (e.g. vomit-induction, laxatives, diuretics, appetite suppressants, excessiv e exercise). Morbid fear of fatness. Body weight higher than required for the diagnosis of anorexia. \200 Repeated vomiting and/or laxative abuse may result in serious electrolyte disturbance, seiz ures, tetany, haematemesis, or stomach rupture. Management Usually best managed by a multidisciplinary team and including the family from t he start. Cognitive behavioral therapy including educational input about healthy eating, st arvation, and binging. Motivational interviewing and family therapy can also be helpful. Ph armacotherapy, e.g. \202 uoxetine, rarely used, but may reduce food craving. Prognosis Full recovery occurs in up to 50% of cases. Between 66 \200\22375% show at least partial recovery at 10-yr follow up. Bone density follow up shows no oste- openia or osteop orosis in recovered bulimic patients. 16_McClure_16.indd 596 11/14/2012 3:42:48 PM BULIMIA NERVOSA 597 16_McClure_16.indd 597 11/14/2012 3:42:48 PM CHAPTER 16 Child and family psychiatry 598 Oppositional de \201 ant and conduct disorders Oppositional de \201 ant disorder (ODD) an d conduct disorder (CDD) are related disruptive behavior disorders, typi \201 ed by de \201 ance, disobedience, and violation of social rules and the rights of others. Epidemiology \200 Prevalence varies greatly depending on the age of the sample and the diagnostic criteria us ed. Both CDD and ODD are more common in males. ODD is more common in younger children (<10y rs). ODD prevalence in 5 \200\22310yr olds is around 4.8% boys and 2.1% girls. CDD prevalen ce increases with age: adolescents. \200 \200 \200 71% in children and 4% in Causes Longitudinal studies of delinquency suggest the causes are complex. Many are likely to have an underlying genetic vulnerability and an association with various pre- and perina tal risk factors. Subsequent exposure to coer- cive parenting (intrusive parenting and subs equent reinforcement of child counterattack and parent withdrawal) early in life has also b een implicat- ed. Later involvement of vulnerable individuals with a deviant peer group pre dicts a CDD pathway as does a variety of psychosocial risk factors, e.g. low socioeconomic status, peer relationship dif \201 culties, parental mental illness, and child maltreatmen t, neglect, and abuse. Clinical features The name ODD is highly descriptive, i.e. hostile, negativistic, and de \201 ant, particularly to the parents. The de \201 ant behavior pattern must last at least 6mths and cause impairment across a variety of domains. CDD is de \201 ned by more seriou s aggressive behavior and rule violations, property dam- age, theft, arson, truancy, and ru nning away, which again must have been present for at least 6mths and result in functional dif \201 culties. Differential diagnosis Comorbidity with other disruptive behavior disorders is common, e.g. ADHD (b p.600). Speech and language de \201 cits may be comorbid or on a causal pathway. Management Prevention is the best approach. Early intervention with ODD in very young child ren using universal parenting programs targeting coercive parenting and parental abuse is i ndicated. If ODD and CDD are estab- lished, programs that employ intensive interventions th at involve children, parents, and other participants in the child \200\231s social ecology have proved effective.1 Multisystemic therapy is an example of such an inter- vention. Reme dial education is likely to be needed and can also be helpful as self-esteem rises. 16_McClure_16.indd 598 11/14/2012 3:42:48 PM OPPOSITIONAL DEFIANT AND CONDUCT DISORDERS 599 Psychopharmacology research on disruptive behavior disorders, other than ADHD, presently provides no de \201 nitive guidelines. \200 \200 \200 ADHD comorbidity should be treated. Planned, premeditated aggression is not an indication f or drug therapy. Impulsive aggression or aggression in an individual with prominent affecti ve symptoms may prove responsive to a 5-HT blocking agent or an atypical antipsychotic (e.g . risperidone). Further research is required before these pharmacological strategies can be demonstrated to be both safe and effective enough to be used in routine clinical practice. Prognosis Management of established disruptive behavior disorders is dif \201 cult. Childr en often fail at school. Poor prognosis with ODD is associated with; \200 \200 \200 early onset of symptoms; longer duration of symptoms; comorbid mood, anxiety, ADHD, impulse control and substance use disorders; development of conduct disorder. Two patterns of CDD are described. Early onset- (onset before the age of 11yrs) and adolesc ent onset-CDD. Whilst adolescent onset CDD is most often self-limiting and does not typical ly persist into adulthood, early onset CDD is associated with a particularly poor prognosis . This is also the case for conduct disorder which is comorbid with ADHD. Almost 50% of all youths that initiated serious violent acts before the age of 11 con- tinued this type of o ffending beyond the age of 20 twice the rate of those who started in adolescence. Approxima tely 40% of prepubertal children with conduct disorder may develop antisocial personality d isorder and most antisocial adult report a history consistent with conduct disorders as a c hild.2 References 1 National Institute for Health and Clinical Excellence (2006). Parent-training/ education pro- grammes in the management of children with conduct disorders. London: NICE. M http://guidance. nice.org.uk/TA102/Guidance/pdf/English 2 Farrington DP. (1998). Predictors, causes and correlates of youth violence. In: Youth vio lence Tonry M, Moore MH (eds). Chicago: University of Chicago Press. 16_McClure_16.indd 599 11/14/2012 3:42:48 PM CHAPTER 16 Child and family psychiatry 600 Attention de \201 cit hyperactivity disorder ADHD is a complex neurodevelopmental disorder . Prevalence Rates of diagnosis vary greatly both between and within different coun- tries. I n the US, Netherlands, and Germany, rates are much higher than in the UK, which is much hig her than those in France, Italy, and Spain. A recent systematic review identi \201 ed 102 studies, across all world regions. Overall prevalence of ADHD was 5.3 %. Prevalence for chi ld- ren 6.5% and for adolescents 2.7%. ADHD is 2 \200\2233 times more common in boys. Preva lence decreases with increasing age. Differences between studies mainly accounted for by th e use of differing diagnostic criteria, the source of information used to elicit symptoms a nd whether impairment was required to be present in order for the diagnosis to be made. Aft er adjustments were made to account for these methodological issues, the prevalence in Nort h America and Europe were similar. Causes ADHD displays considerable heterogeneity at the genetic, pathophys- iological, cogni tive, and behavioral levels of analysis. Whilst the exact etiology of ADHD is unknown consi derable research supports a strong genetic component (heritability of 0.7) with non-shared environmental factors contributing most of the residual variance. Environmental fac- tors a re likely to include prenatal exposure to nicotine, pre and perinatal obstetric complicatio ns and low birth weight, exposure to lead and other environmental toxins. Gene-environment interactions seem likely to be particularly important, but have not yet been studied extens ively. Diagnostic criteria \200 Inattention: \200 \200 \200 \200 \200 Hyperactivity: \200 \200 \200 \200 \200 Impulsivity: \200 \200 \200 e.g. fails to attend to detail; dif \201 culty sustaining attention; does not follow throu gh; dif \201 culty organizing tasks, easily distracted; reluctant to engage in tasks that require sustained mental effort. e.g. often \201 dgets; leaves seat in classroom; runs and climbs excessively; often on the go; acts as if driven by a motor. e.g. often blurts out answer before the question has \201 nished; has dif \201 culty waiting turn; interrupts and butts in. Symptoms must be present for at least 6mths, be present before age 7yrs, and result in impa irment in 2 or more functional domains or settings. In DSM-IV inattentive, hyperactive \200 \223impulsive, and combined subtypes are described. The ICD-10 criteria are more restrictiv e and only include those 16_McClure_16.indd 600 11/14/2012 3:42:48 PM ATTENTION DEFICIT HYPERACTIVITY DISORDER 601 with severe, pervasive and impairing combined ADHD in the diagnostic category hyperkinetic disorder. This results in a lower prevalence for hyper- kinetic disorder of around 1.5%. Di fferential diagnosis In young children it may be dif \201 cult to differenti- ate age-appr opriate boisterousness and activity from ADHD symptoms. Inattention may be due to under-sti mulation of above-average children or seen in children in classroom settings too advanced f or their mental age. ADHD symptoms common in PTSD (b p.586) and autism spectrum disorders ( b p.602). Common comorbidities \200 b p.598; Disruptive behavior disorders (ODD and CDD) (see 42 \200\22368%). Anxiety (22 \200\22337%). Depression (12 \200\22317%). Learning, speech, and language disorders are also overreprese nted. \200 \200 Treatment \200 Psychopharmacology: (methylphenidate, dexamfetamine) and the non-stimulant atomoxetine. Beh avioral interventions: integrated home \200\223school behavior management, token economies, and parent effectiveness training. The effectiveness of family interventions is inconclusi ve. drug therapies include psychostimulants A multisite randomized controlled trial (NIMH-MTS study) of combined subtype ADHD found tha t, over 14mths, carefully organized medication was superior to either behavioral treatment or community care (which usually included less well organized medication treatment) for cor e symp- toms and that a combination of behavioral and medication therapies were equally bet ter for related symptoms compared with usual care.1 Current UK2 and European practice suggests that for those, over 6yrs of age, where ADHD is severe, pervasive, and impairing ADHD (ICD-10 hyperkinetic disorder) medication will usuall y be the \201 rst choice treat- ment. For those with less severe ADHD behavioral interven tions are suggested as the \201 rst choice treatment with medication reserved for those w ho either fail to respond to the behavioral treatments or for whom behavioral treatment is not possible. Prognosis \200 \200 \200 70 \200\22380% continue to display symptoms and impairments as adolescents. 50 \200\22365% as adults. Only 10 \200\22320% reach adulthood without any psychiatric diagnosis, functioni ng well, and without symptoms of their disorder. Pharmacological treatments may be continue d into adulthood Reference 1 See reference list at: M http://www.rcpsych.ac.uk/mentalhealthinfo/mentalhealth and growin- gup/adhdhyperkineticdisorder.aspx 2 National Collaborating Center for Mental Health (2008) The NICE guideline on diagnosis an d management of ADHD in children, young people and adults. London: British Psychological So ciety and Royal College of Psychiatrists. M http://guidance.nice.org.uk/CG72/Guidance/pdf/E nglish 16_McClure_16.indd 601 11/14/2012 3:42:48 PM CHAPTER 16 Child and family psychiatry 602 Autism spectrum disorders Disorders in this cluster, also called pervasive developmental di sorders (PDD), have common clinical features in the areas of communication, social relatedn ess, movement, and intrapersonal relations. Nosological issues include the diagnostic disti nctiveness of syndromes and whether presentations can change over time. Autism spectrum dis orders include: \200 \200 \200 71/1000). Autism (prevalence Rett \200\231s syndrome (prevalence 1/15 000). Asperger \200\231s disord er (prevalence 3 \200\2234/1000). Etiology It is likely that the autism spectrum disorders are heterogeneous in aeti- ology. Most believe there are underlying complex genetic vulnerabilities with subsequent environme ntal in \202 uences and factors that trigger gene expression. Recent functional neuroimagi ng studies have led to a wide variety of neurobiological hypotheses. It is likely numerous neural systems are involved with a focus on areas typically implicated in emotional regula- tion such as the limbic lobe. (See references for Cochrane reviews discuss- ing bene \201 t of diet, vitamins, and auditory integration training.1 \200\2233) Clinical features \200 Usually identi \201 ed in the pre-school years, but may be found later in individuals with above average IQ. Problems with social interactions include appearing aloof, impaired non- verbal behaviors, dif \201 culty establishing friendships, and poor or absent emotional re ciprocity. Language problems include marked delay of or lack of speech, inability to conver se, and abnormal speech including stereotypical speech. Behavior problems include preoccupi ed, stereotypical behaviors (e.g. hand \202 apping). In adolescence aggressiveness, mood variability, and sexually inappropriate behavior can be problematic. Mental retardation, la nguage delay, ADHD, and medical complications such as epilepsy often coexist with an autism spectrum diagnosis. Management No single intervention appears superior. Psychosocial interventions, of- ten wit h an emphasis on behavior management and parent involvement, can often lead to increased ch ild skills and have high parent satisfaction. However, such improvement does not usually le ad to signi \201 cant changes either on standardized measures or improve the overall devel opmental trajectory. Recent studies with atypical neuroleptics (e.g. risperidone) hold much promise for improvement of global functioning. For an in-depth dis- cussion of recent asse ssment, aetiological, and treatment research.4 Prognosis \200 \200 \200 70% remain severely handicapped. 50% develop useful speech. 5% will lead independent adult lives. 16_McClure_16.indd 602 11/14/2012 3:42:48 PM AUTISM SPECTRUM DISORDERS 603 References 1 Millward C, Ferriter M, Calver S, et al. (2004). Gluten and casein-free diets for autistic spectrum disorder. Cochrane Database Syst Rev 2004;(2):CD003498. 2 Nye C, Brice A. (2002). Combined vitamin B6 \200\223magnesium treatment in autism spectru m disor- der. Cochrane Database Syst Rev 2002;(4):CD003497. 3 Sinha Y, Silove N, Wheeler D, et al. (2004). Auditory integration training and other soun d thera- pies for autism spectrum disorders. Cochrane Database Syst Rev 2004;(1):CD003681, publ. 2. 4 Volkmar FR, Lord C, Bailey A, et al. (2004). Autism and pervasive developmental disorders. J Child Psychol Psychiat 45(1): 135 \200\22370. 16_McClure_16.indd 603 11/14/2012 3:42:48 PM CHAPTER 16 Child and family psychiatry 604 Individual psychotherapy All health professionals working with children talk to the childre n by themselves sometimes. All try to be helpful, and probably most of us are helpful at le ast some of the time. So in what way is psychotherapy differ- ent from an informal helpful chat? Perhaps the key elements are that the treatment is delivered by a trained therapist w ho carries out therapy with- in a theoretical framework. There are a wide range of individu al therapies including the following. Behavior therapy This is brief and is directed at encouraging desired behaviors and the eli minating problem behaviors. Problems are dealed within a behavioral framework rather than t hrough focus on underlying thoughts, feelings, or past causes. Cognitive behavior therapy As above, but with a wider focus on thoughts and attribution of mean- ing, as well as behavior. This is one of the better researched therapies, though ther e remains a shortage of trained therapists. CBT involves the keeping of diaries and homewor k carried out between sessions. Psychodynamic psychotherapy Longer-term treatment directed at underlying problems and the p resent- ing symptom. Central to treatment are theories of the unconscious mind. The patient is encouraged to use their relationship with the therapist to explore dysfunctional patter ns of behavior. The therapist is able to com- ment on these and help the patient to underst and new ways of relating. Therapy in the younger age group may be based more around play ma teri- als such as animals, crayons, and paper. Just to complicate matters there are also pl ay therapists who are not necessarily psychodynamic in their orientation. Which therapy is best? The inevitable question arises as to which therapy is better. It is dif \201 cult to answer as short therapies directed to diagnostic related groups are easie r to evaluate. In particular there is a growing body of evidence to support the use of CBT in a range of conditions. That being said it is also probably true those well motivated, in telligent, articulate patients without previous problems and from well functioning families are likely to do better with whichever therapy. Non-speci \201 c factors about therapists (e.g. empathy, good listening, and warmth) may be pre-requisites to effective treatment wh atever the model. 16_McClure_16.indd 604 11/14/2012 3:42:48 PM FAMILY THERAPY 605 Family therapy This term covers a wide range of treatments with a similar diversity of theo retical underpinnings. They share the idea that problems are affected by the communication between family members and such communication can serve to maintain or to ameliorate their dif \201 culties. One of the points of difference concerns understanding of the prob- lem. Family therapy bas ed on systems theory might identify recurring dys- functional patterns of interaction and t ypically might hypothesize that the presenting problem in one family member is a manifestat ion of this. Such a view, of pathology being located between, rather than within people, ma y be at odds with the Western focus on the individual. An example of such an approach is th e school-refusing child who is being kept home to act as a buffer between parents who are i n con \202 ict. The child \200\231s presence may prevent dangerous escalation, but may als o interfere with the parents \200\231 ability to resolve their differences. Therapy in this case might focus on helping the parents to address their dif \201 culties without involve ment of the child, and for the child to trust his/her parents to do this and to get on with being a child, e.g. going to school. An alternative is to help the family members to be aware that they are feeling overwhelmed by the problem, have lost con \201 dence, and are not seeing that they do have the resourc es to deal with it. They might be helped to think of occasions when they have overcome dif \201 culties without the help of their child; or to see how they do this and more often. T he child may be helped to see that he/she does, at times, overcome his/her fear and gets on with being a child, and can do more of this. Finally, we can consider family therapy for multifactorial illnesses, such as autism. This is not a product of any particular family pattern or dysfunc- tion. However, this does not mean that the family cannot be helped to manage this better. Such an approach is likely to focus on support, on psycho-education, and on helping the family to address the development al (independence) issues, which are there for any family, but so much more dif \201 cult w hen there is a child with chronic illness or disability. Outcome The heterogeneity of family therapy, the wide variety of problems it is used to add ress, and sometimes an overemphasis on complex theory that can seem a long way from clinica l practice have contributed to a dearth of outcome research. There is evidence though for e ffectiveness in a range of conditions including anorexia nervosa (AN) (see b p.594). Contraindications Non-clinicians often see family therapy as a potential panacea for all fa m- ily based problems. Unfortunately this is not the case and family therapy is not always the correct way to address such dif \201 culties. Family therapy is not possible if the fa mily cannot, or will not, attend. It is contraindicat- ed in families where one member is b eing severely scapegoated. Unless there is reason to believe that such a family is open to the idea of doing things differently once this pattern is identi \201 ed, family therapy s hould be discontinued. 16_McClure_16.indd 605 11/14/2012 3:42:48 PM CHAPTER 16 Child and family psychiatry 606 Psychopharmacotherapy Societal views exist about medication for mental health in general an d speci \201 cally for children. Not all mental health professionals hold positive views a bout psychoactive medications or believe them to be safe and effective treatments for menta l health disorders. Some non-professional groups are openly antagonistic. Whilst there is s ome clear evidence to support the use of medications for some children and adolescents with some disorders in some situations, it is also true that more research and stronger evidenc e is urgently required. Until recently prescribing for children and adolescents with mental health problems has not bene \201 ted from age-speci \201 c pharmacokinetic studies, nor had there been extensiv e work establishing the pharmaco- dynamics of psychoactive medications. As a consequence fo r almost all psychopharmacological situations, other than ADHD, one usually assumes that th e pharmacodynamic effect in children is the same as that in adults. Similarly, there has be en relatively little attention paid to pharmacoviga- lence and many questions about drug sa fety remain unanswered. Data supporting ef \201 cacy and effectiveness also remain relatively sparse and the curre nt evidence-based medicine summaries do not comprise a comprehensive review of child and ad olescent mental health prescribing (see Cochrane Library). Many protocols are listed; over time it is hoped there will be more consistent coverage from completed reviews. Despite thi s lack of evidence, psychotropic medication prescribing has increased exponentially over th e past 15yrs. Fortunately, recent changes in legisla- tion in the US and Europe have meant that far more psychiatric drugs are being trialed and licensed for use in children. For speci \201 c prescribing information, indications, contraindications, pre- cautions, s ide-effects, and dosage regimes the reader should consult an up-to-date formulary and the p rimary literature. One reference text offers the following useful headings in a section on general principles.1 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 First do no harm. Know the disorder and use drugs when indicated. Choose the best drug. Und erstand the drug and its properties. Minimize drug use and dosage. Keep things simple. Avoi d polypharmacy. Don \200\231t be a \201 ddler or follow fads. Take particular care with c hildren. Establish a therapeutic relationship. Compliance (adherence) with treatment. Whilst some mild mental health presentations may respond to medica- tion alone, in individu als with multiple comorbidities, impairment across domains, or distressed parents, medicati on is almost invariably adjunctive to or part of a more comprehensive and sophisticated man agement plan. Reference 1 Werry JS, Aman MC. (1999). Practitioner \200\231s guide to psychoactive drug fo r children and adolescents, 2nd edn. New York: Plenum Medical Book Co. 16_McClure_16.indd 606 11/14/2012 3:42:48 PM 607 Chapter 17 Hematology Peripheral blood \201 lm 608 Anemia 610 Haemolytic anaemias 612 De \201 ciency anaemias 614 Red blood count membrane defect anaemias 616 Red blood count enzyme defect anaemias 618 Sickle cell disease 620 Thalassaemia 622 Immune haemolytic anemia 624 Red blood cell fragm entation 625 Aplastic anemia 626 Failure of red cell production (pure red cell aplasia) 628 Polycythaemia 630 Abnormal bleeding or bruising 632 Coagulation studies 634 Disseminated i ntravascular coagulation 635 Hemophilia A 636 Hemophilia B 637 von Willebrand disease 638 P latelet function disorders 640 Thrombocytosis 641 Thrombocytopenia 642 Acute immune thrombo cytopenia 643 Thrombophilia 644 Blood transfusion 646 Blood transfusion reactions 648 17_McClure_17.indd 607 11/14/2012 3:50:12 PM CHAPTER 17 Hematology 608 Peripheral blood \201 lm Table 17.1 FBC and blood \201 lm abnormalities and their causes Abnormality Cause(s) Acanthocytes Abetalipoproteinaemia, severe liver disease, Vitamin E de \201 ciency in premature neonate s, hereditary acanthocytosis Basophilia Myeloproliferative disorders, chronic myeloid leukemia (CML), basophilic leukemia, reactive disorders, e.g. ulcerative colitis, infection Basophilic stippling Ineffective erythropoiesis; haemoglobinopathies, recovering bone marrow, lead poisoning Echinocytes (Burr cells) Renal failure, pyruvate kinase de \201 ciency, liver disease, HUS, burns Hereditary ellipt ocytosis (b p.616) Parasitic infections, allergic states, e.g. asthma, eczema, drugs, polya rteritis Elliptocytes Eosinophilia Fragmented red blood cells (RBC) Microangiopathic and mechanical haemolytic anaemias, DIC (b p.625), HUS (b p.376), renal fa ilure G6PD de \201 ciency (b p.618), haemoglobinopathies, post-splenectomy, hyposplenism, Heinz body haemolysis Heinz bodies (intracellular Hb precipitate) Howell \200\223Jolly bodies (intracellular DNA fragments) Normal neonatal blood picture, hyposplenia, post-splenectomy, megaloblastic anemia Leukemia (b p.656) Infection, mainly viral, malignancy, stress, vomiting, burns, anorexia, drugs, S LE, Crohn \200\231s disease, immunode \201 ciency states (SCID, diGeorge syndrome, acquire d, e.g. HIV), marrow failure, aplastic anemia, leukemia Leucocytosis Lymphocytopenia (lymphopenia) Lymphocytosis Viral and non-viral (pertussis, mycoplasma, malaria) infection, leukemia, atypical lymphocy tosis (EBV, CMV, adenovirus), stress, exercise, status epilepticus Vitamin B12 or folate de \201 ciency (b p.615), aplastic anemia (b p.626), normal neonatal blood picture (b p.192) Iron de \201 ciency (b p.614), thalassaemia (b p.622), anemia of chronic disease Macrocytic RBCs Microcytic RBCs Monocytopenia Autoimmune disorders, e.g. SLE, drugs, e.g. corticosteroids, chemotherapy Monocytosis Chronic bacterial infection, malaria, typhoid, TB, infective endocarditis, post-chemotherap y See b pp.627, 724 Neutropenia 17_McClure_17.indd 608 11/14/2012 3:50:12 PM PERIPHERAL BLOOD movie 609 Neutrophilia Infection, in \202 ammation, chronic bleeding, post- splenectomy, drugs, e.g. corticostero ids Reticulocytosis/polychromatic RBCs Haemolysis, bleeding, response to haemotinics (e.g. iron), marrow in \201 ltration Sickle cell anemia (b p.620) Normal neonatal blood picture, hereditary spherocytosis (p.616), immu ne mediated haemolytic disease, post-splenectomy Severe iron de \201 ciency (b p.614), sic kle cell disease, thalassaemia, liver disease, post- splenectomy, asplenia See b pp.642 \200\223643 See b p.641 Sickle cells Spherocytes Target cells Thrombocytopenia Thrombocytosis 17_McClure_17.indd 609 11/14/2012 3:50:12 PM CHAPTER 17 Hematology 610 Anemia Red cell indices vary considerably with age. Hemoglobin (Hb) at birth may be as high as 22g/dL, but then falls rapidly to about 11g/dL by 3mths. A mild hypochromic microcytic picture normally seen between 6mths and 6yrs. Sex differences in red cell indices do not ap pear until puberty. Symptoms and signs of anemia \200 \200 \200 \200 \200 \200 Fatigue, lethargy. Pallor. Poor feeding, anorexia. Poor growth. Dyspnoea on exertion. Rarel y stomatitis or koilonychia. Diagnostic approach to anemia History \200 \200 \200 \200 \200 Familial/ethnic causes (sickle cell, thalassaemia). Diet (cow \200\231s milk, vegan). Overt blood loss. Duration of symptoms. Drug history, e.g. NSAIDs. Examination \200 \200 Height and weight (FTT, malabsorption). Dysmorphic features, e.g. micrognathia, cleft palat e, abnormal/absent thumbs (Fanconi \200\231s anemia, Diamond \200\223Blackfan anemia). Jaun dice (haemolysis). Adenopathy/organomegaly (underlying malignancy). \200 FBC and \201 lm (See Table 17.2) \200 Red cell indices: mean cell volume (MCV), mean cell hemoglobin (MCH), mean corpuscular hemo globin concentration (MCHC) (anemia may be microcytic, macrocytic, normocytic, and/or hypoc hromic). RBC: Other cytopenias. \200 spherocytes, sickle cells, Howell Jolly bodies. 17_McClure_17.indd 610 11/14/2012 3:50:12 PM anemia 611 Table 17.2 Investigations for different anemia types Anemia type Investigate for Microcytic anemia Iron de \201 ciency, thalassaemias, sideroblastic anaemias, anemia of chronic disease Macrocytic anemia Bone marrow failure syndromes (reticulocytopenic anaemias; pure red cell aplasia, aplastic anemia, Diamond \200\223Blackfan anemia), myelodysplastic syndromes, megaloblastic anemia ( B12/folate de \201 ciency), dyserythropoeisis, drugs Normocytic anemia Haemolysis, sequestration, anemia of chronic disease, recent signi \201 cant bleeding, combined iron and B12/folate de \201 ciency, i.e. severe malnutrition Inves tigate as described on b p.612 Haemolytic anemia 17_McClure_17.indd 611 11/14/2012 3:50:13 PM CHAPTER 17 Hematology 612