Download Treatment - Google Groups

Week 1-2: SHOCK (Hypovolaemic Shock)
Definition
Shock is the syndrome (a constellation of symptoms and signs) that results from reduced perfusion
(blood flow) to the tissues of the body.
Pathogenesis
Shock is the final common pathway for a number of potentially lethal clinical events, including severe
haemorrhage, extensive trauma or burns, large MI, pulmonary embolism and microbial sepsis. Shock
has many causes that can be grouped:
(i) Cardiogenic: shock due to myocardial pump failure – MI, ventricular arrythmias, outflow
obstruction (pulmonary embolism),
(ii) Hypovolaemic: shock due to deficient circulating blood volume – significant haemorrhage, fluid
loss from severe burns,
(iii) Distributive/Toxic: shock due to expansion of the volume of the vascular system without a
corresponding increase in the circulating blood volume – systemic microbial infection.
Clinical Features
The usual signs are a weak rapid pulse (due to low blood pressure and rapid heart rate), cool, clammy
cyanotic skin, with the patient experiencing symptoms of air hunger and a feeling of impending doom.
Morphology
Regardless of its underlying pathology, shock gives rise to systemic hypoperfusion caused by reduction
in either CO or circulating blood volume. The end results are hypotension, followed by impaired tissue
perfusion and cellular hypoxia. Although hypoxic and metabolic effects of hypoperfusion initially cause
only reversible cellular injury, persistence of shock eventually leads to irreversible tissue injury and
death.
Hypovolaemic Shock Morphology
blood volume  systemic filling pressure   venous return  CO  tissue perfusion. If
about 10% of the blood volume is lost, compensatory mechanisms may be adequate but after a greater
blood loss, shock may progress irreversibly  death.
Compensatory mechanisms include:
Short term - seconds to minutes in onset
 Autoregulation
 Increased sympathetic activity from baroreceptor reflex with reflex tachycardia and
vasoconstriction (except brain & heart, most marked in skin, kidneys)
 Central ischaemic response (if mean arterial pressure <50-60mmHg)
Medium term - minutes to hours in onset
 Fluid redistribution from tissues back into capillaries
 Circulating vasoactive substances
o adrenaline/ noradrenaline
o vasopressin
o angiotensin II/ aldosterone
Long term - continuing for days
 Restoration of salt and water balance through
o kidney response
o thirst
o hormonal activity
o erythropoiesis
Treatment
 IV fluids – colloids (fluid with protein products) and crystalloids (Saline)
 O2 admin
 Rx cause – haem
Blood Loss
Short term comp
Med term comp
Long term comp
MAP
CO
TPR
SNS Activity
VC
SV
HR
Venous Ret
SNS Activity
Blood
Viscosity
# of RBC
Local Metabolic Control
Respiratory
Activity
Shivering
Blood Vol
Vasopressin &
Angiotensin II
Fluid shifts
into caps
NaCl and H2O Balance
Vasopressin
& RAAS
Erythropoiesis
Week 3: ACNE
Definition & Epidemiology
Acne is a reasonably common facial rash occurring in adolescence and sometimes into early adult life.
It is seen in both males and females, but males tend to suffer from more severe forms of the disease.
Other Useful Definitions
Macule: Circumscribed lesion of up to 5mm in diameter, characterized by flatness.
Papule: Elevated dome-shaped or flat-topped lesion 5mm or less across.
Nodule: Elevated lesion with spherical contour greater than 5mm across.
Vesicle: Fluid filled raised lesion 5mm or less.
Bulla: Fluid filled raised lesion greater than 5mm across.
Pustule: Discrete, pus filled, raised lesion.
Wheal: Itchy, transient, elevated leasion with variable blanching and erythemo formed as the result of
dermal oedema.
Scale: Dry, horny, platelike excresence; usually DT imperfect cornification.
Excoriation: traumatic lesion characterized by breakage of epidermis causing raw linea area (often self
induced).
Erosion: Discontinuity of the skin exhibiting incomplete loss of epidermis.
Ulceration: Discontinuity of the skin exhibiting complete loss of epidermis, often portions of dermis and
even subcutaneous fat.
Pathogenesis
Four key components contribute to the development of acne:
1. Changes in keratinisation of the lower portion of the infundibulum with the development of a
keratin plug blocking outflow of sebum to the skins surface,
2.  size of sebaceous glands with puberty or  activity DT hormonal stimulation,
3. Propionibacterium acnes – lipase-synthesising bacteria colonising the hair follicle, converting
lipids in sebum to pro-inflammatory fatty acids,
4. Inflammation in the follicle associated with the release of cytotoxic and chemotactic factors
The above components may be induced or exacerbated by drugs (corticosteroids, testosterone,
contraceptives), occupational contactants (Macca’s), occlusive conditions including heavy clothing and
tropical climates.
Clinical Features
 Acne presents in areas rich in sebaceous glands – face, back and sternal areas.
 The skin may appear greasy and inflamed
 Deep-seated nodulocystic lesions and dermal inflammation can cause acne scarring
Morphology
Divided into non-inflammatory and inflammatory types:
 Infalmmatory – Erythematous papules, nodules and pustules
 Non-inflammatory – Open comedones (blackheads: follicular papules with central black plug –
black DT oxidation of melalin pigment) and closed comedones (whiteheads- follicular papules
without central plug). May lead to inflam type.
Extensive acute and chronic inflammation accompanies follicular rupture. Dermal abscesses may form
in association with the rupture.
Treatment
Aimed at:
  Sebum Production



 bacteria
 inflammation
Normalising duct keratinisation
Rx CLASS
Topical
Retinoids
Topical
Antibiotics
BPO (Benzoyl
Peroxide)
Oral Antibiotics
Hormonal
Therapy (OCP)
Keratolytic
(Salicylic acid &
sulphur-based)
ACTION
EXAMPLE
Inhibit microcomedo formation by reg the follicular keratinocyte.
Normalise keratinocyte desquamation by affecting follicular turnover
and cell maturation. Anti-inflam properties affecting immune response,
inflam cell migration & mediators.
Reduce bacterial infection but problems with resistance common
Help to resolve inflammatory acne
Most potent topical antimicrobial with rapid bactericidal action
resulting in rapid reduction in bacterial organisms.
Cause a reduction in resident skin bacteria, P acnes and Staph
epidermidis. Also have intrinsic anti-inflam properties
Decrease the amount of circulating androgens which in turn results in a
decrease in sebum production
These preparations are keratolytics (peeling agents) that can unblock
pores by removing keratin plugs.
Cytokine production
Neutrophil recruitment
Rupture of sebum
in dermis
Inflammatory Pustule
Papule
Protease production & hydrolysis
of lipids to proinflam fatty acids
Comedone
Tretinoin
Adapalene
Tazarotene
Clindamycin
Many diff formulations
washes1-10%
Tetracycline, Doxycycline
Minocycline
Diane
Juliet
Clearasil
DermaVeen
 Propionibacterium acnes
Pilosebaceous duct blockage
 Sebum production DT
sebaceous hyperplasia
Pilosebaceous duct
hypercornification
 Androgens in puberty
Genetic susceptability
Week 4: SCID
Definition and Epidemiology
Severe combined immunodeficiency disease (SCID) represents a constellation of genetically distinct
syndromes all having common defects in both humeroal and cell-mediated immune responses. More
common in boys.
Pathogenesis
SCID is a primary immunodeficiency disorder determined by genetics. The most common form is Xlinked (The reason why more boys suffer from SCID) but autosomal recessive defects also cause the
disease.
 X-linked – Profound defect in the earliest stages of lymphocyte development especially T-cell
development. T-cell numbers are greatly reduced and although B-cell numbers are normal
antibody synthesis is impaired DT lack of help form T-cells.
 Autosomal Recessive – Deficiency in enzyme Adenosine Deaminase causing accumulation of
toxic products that affect immature lymphocytes, esp T-cells. Greater reduction in T-cell
numbers than B-cell numbers.
Clinical Features
Affected infants present with prominent thrush, nappy rash and failure to thrive.
Morphology
 SCID pts are extremely susceptible to recurrent, severe infections by a wide range of pathogens.
 Hypoplastic lymphoid tissue.
Investigations
Blood tests and histology of lymph tissue
Treatment
Without a bone marrow transplant death usually occurs in the 1st year of life.
Other Primary Genetic immunodeficient Dzs
 Hyper IgM syndrome – Functionally abnorm T-cells
 DiGeorge Syndrome – T-cell deficiency DT failure of d’ment of pharyngeal pouches –
hypoplasia of thymusGenetic deficiency of complement system
Failure to Thrive
The following diagnostic criteria have proved helpful in identifying inadequate weight gain in infants:
1: Failure to regain birth weight by 3 weeks of age.
2: Weight loss of greater than 10% of birth weight by 2 weeks of age.
3: Weight dropping below the third percentile.
4: Deceleration of growth from a previous established pattern of weight gain.
5: Evidence of malnutrition on examination, eg) min subcutaneous fat or wasted buttocks.
Week 5: HEPATITIS
Definition
Viral hepatitis applies to liver infections resulting in inflammation caused by several unrelated viruses.
Viral Agent
Hep A
Enterovirus
Hep B
Hepadna virus
Hep C
Unclassified
Transmission
Faecal-oral
Incubation
Type
2 – 6 wks
Acute or
inapparent
None
Parenteral/
close contact
2 – 26 wks
Acute or
persistent
>50%
No
Parenteral/
close contact
4 – 26 wks
Acute or
persistent
5-10% of acute
infects
Yes
Yes
Hep D
RNA genome
Hep B capsid
Parenteral/ close
contact
4 – 7 wks
Acute or
persistent
80% on
superinfect
Yes
No
Yes
Yes
Yes
No
Yes
Yes
No
HBV Vaccine
No
Chronic
Hepatitis
Carrier State
Hepatocellular
carcinoma
Vaccine
Hep E
Unclassified
Waterborne/
Faecal-oral
2 – 8 wks
Acute or
inapparent
None
No
Pathogenesis
Damage to liver is due to a two-fold mechanism:
1. Virus injures liver cells directly (Remember: APUTRAR)
2. Virus triggers a host immune response which then causes inflammation and attack of liver cells
by cytotoxic T-cells
Clinical Presentation
 Can show a range of symptoms (Mostly GIT)– Bile in urine, pale stools, jaundice, anorexia,
mailase, nausea and vomiting as well as a low grade fever.
 HAV may be asymptomatic
 HBV may also present with a rash and joint px
Serology
+ Result Indicates
Details
HAV-Ag
Hep A viral Antigen
Present only during acute infection (wks 2-6)
HAV-IgM
Early Antibodies – Acute infection
Appear early @ same time of symptom onset
HAV-IgG
When NO IgM: Previous exposure OR
vaccination
IgG provides lifelong immunity against infection
HBsAg
Active infection & current carrier
Anti-HBs
HBeAg
Immunity via previous infection or
immunisation
acute, chronic/ resolved infection. NOT
marker of vaccine-induced immunity
Active Viral Replication
The surface antigen of HBV. Usually appears a few weeks
PRIOR to symptoms, disappears during covalescence
Antibody to the surface antigen. It usually appears AFTER
the clinical illness and persists for life.
Antibodies to the core antigen
HBV DNA
Active Viral Replication
Hep A
Hep B
Anti-HBc
Antigen derived from the viral core. Ass with  infectivity
&  risk of developing chronic Dz
Genome of HBV
Hep C
Anti HCV
Acute/ chronic infection or immunity
RT-PCRHCV
Current infection
Antibodies against the HCV virus. +ve result indicates
exposure but doesn’t indicate if infection is present now
This test is nec to tell if there is a current infection
Acute Hepatitis
Four phases:
1. Incubation period: peak infectability occurs in the last few days of the incubation period,
2. Symptomatic preicteric phase: non specific symptoms – malaise, fatigue, nausea,  appetite,
fever, headaches, muscle and joint aches,
3. Symptomtic icteric phase: Jaundice, pale stools and dark urine all caused by conjugated
hyperbilirubinemia along with mildly enlarged, moderately tender liver,
4. Convalescence: Recovery is via generation of a strong T-cell response to viral antigens
expressed on infected liver cells.
Treatment/Management
 Provide adequate nutrition,
 Prevent further damage to the liver (eg OH, drugs etc),
 Prevent spred of infection to others (Hygiene, sexual activity etc)
Fulminant Hepatitis
Rarely, cases of acute hepatitis can deteriorate rapidly and cause massive liver necrosis and atrophy.
Only Rx is an emergengy liver transplant.
Hepatitis Complications
 Cirrhosis
 Hepatocellular carcinoma
 Ascities
 Liver failure
 Portal hypertension
Week 6: Giardia Lamblia & Diarrhoea
Definition and Epidemiology
Giardia Lamblia is a flagellate protozoan whose colonisation of the small intestine causes malabsorption
and diarrhoea. It is found world wide. Spread (cysts) by faecal-oral route, transmission can be water
borne or through animal vectors. Giardia is generally not notifiable unless there is evidence of an
outbreak – multiple associated cases within a short time frame.
Pathogenesis
Generally Giardia lives on the surface of mucosa, in the mucus layer causing:
 Blanketing over large areas of GI (obstructs absorption)
 DIRECT DAMAGE (release of proteases and endotoxins)  mucous/electrolyte and H20
secretion &  absorption of Na+/H20 (body tries to flush out pathogen)
 There is a structural progression in the damage to the GIT
 1st microvillous disruption   Disaccharidase activity,  Glucose stimulated Na+/Cl/H20 absorption
 Then macrophage activation and Lymphocyte infiltration  villous atrophy and crypt
deepening   absorption and  secretory activity
 Deconjugation of bile salts (bile salts not reabsorbed)  lipid absorption membrane secretion
and steatorrhea
 Inhibition of pancreatic enzymes   b’down and abs of nutrients  malabsorption
 Malabsorption of vit (fat & water soluble), Fe and Amino acids predisposes to anaemia
 Folate deficiency  exacerbate villous atrophy (may need to give supplements)
 Malabsorption  nutrients dumped into lumen  bacterial fermentation + osmotic overload 
diarrhoea
 Pathogenesis and epidemiology is almost identical with Cryptosporidiosis
Life Cycle:
 Ingested cysts  trophozoites (EXcystation) when exposed to stomach acid and intestinal
proteases
 After excystation undergoes binary fission within 30minutes
 Trophozoite  cyst (ENcystatin) occurs at alkaline pH and changes in bile salt concentrations
 Cysts passed into stool
Clinical Presentation (1-3 wk incubation)
 Often asymptomatic (but are still infective)
 Explosive, watery, malodorous stools, cramps, nausea,
epigastric pain, mild fever
 Diarrhoea can be acute (usually 3-4 days, <1 month) or
 Chronic diarrhoea (month to years) and malabsorption (in
50% of chronic cases)
 Brief recurrent episodes of foul, frothy stools
 Steatorrhea (fatty diarrhoea)
 ↓ growth, failure to thrive, weight loss
 Blood and mucus usually NOT present
 Infection leads to development of antibodies against Giardia.
However organism in intestinal lumen  not eaten by phagocytes. Antibodies may neutralise toxin

severity 
Investigations
 Diagnosis of intestinal parasites is usually by identifying characteristic trophozoites/worms or
cysts/eggs in stool
 In giardiasis, parasite numbers in stool may be low and esp. hard to find in chronic cases
 Aspiration and biopsy possible but stool examine is preferred (3 stools should be taken at 2 day
intervals)
 ELISA test also available OR else just TREAT and see.

Stool sample are almost NEVER cultured
Treatment
 Scrupulous hygiene (↓faecal-oral re-infection/transmission)
 Oral rehydration with all diarrhoea
 Metronidazole is drug of choice – 400mg TDS 1/52 (Works by interfering with DNA synthesis)
 Tinidazole is actually the recommended 1st line therapy in AMH (2000mg single dose)
 Health promotion and education aimed at improving personal hygiene, and emphasizing hand
washing, sanitation and food handling, are effective control activities for the reduction of person-toperson transmission.
Week 7: Peptic Ulcer & Helicobacter pylori
Definitions & Epidemiology
Ulcer: (Histologically) a breach in the mucosa of the alimentary tract that extends through the
muscularis mucosa, into the submucosa or deeper.
Helicobacter pylori: A spiral shaped, gram negative, urease producing bacterium. Its ability to colonise
in the acidic stomach env is DT sheathed flagella that allow rapid movement to mucus layer where pH is
higher, and its ability to produce urease - converts urea to ammonia,  the pH directly around th colony.
Peptic ulcer: is a chronic, often solitary lesion that occurs in any portion of the GIT exposed to the
action of acid/peptic juices. There is a high prevalence of H.pylori in developing countries and is ass
with  SES worldwide. Spread is oral-oral or faecal-oral route.
Pathogenesis
Peptic ulcers are produced by an imbalance between gastroduodenal mucosa defence mechanisms and
the damaging forces, particularly gastric acid and pepsin. H.pylori infection is a major contributing
factor to peptic ulcer. H.pylori mechanisms of evil action:
 H.pylori Infection intense inflamm & immune response   production of anti-inflam
cytokines IL1,6,8 & TNF  Recruitment neutrophils activation T & B cells
 H.pylori infection  enhanced gastic acid secertion & impaires bicarb procution by duodenum
 Decrease in luminal pH of duodenum
 H.pylori infection  bacteria secretes Urease  Urea B’down to toxic compounds (including
Ammonia)  Damage to mucus lining and surface epithelial cells
Morphology
Peptic ulcers are usually solitary lesions of 4cm in diameter with 98% located in either the 1st protion of
the duodenum and the antrum of the stomach (Duo:Stom = 4:1).
Clinical Features
 Epigastic gnawing, burning or aching px
 Px tends to be worse @ night and occ usually 1-3 hrs post meals during the day
 Px is relieved with alkalis or food
 In perforating ulcers Px may be referred to the back, left upper quadrant or chest (often misinterpreted as cardiac in origin!!)
 May initially present with complications of anaemia, frank haem or perforation
Investigations
Non-invasive methods:  C13 Urea Breath Test – Quick and easy way to detect presence of H.pylori.
Measurement of 13CO2 in after ingestion of C13 urea
 Serology Tests – IgG antibodies
 Stool Test
Invasive (Endoscopy)  Rapid Urease Test – gastric biopsy tested for urease
 Culture and Histology of gastric biopsy
Treatement
1. Neutralise acid secretion – Antacids (AlOH, MgOH, CaCO3)
2. Inhibit acid secretion – PPIs (Pantoprazole), Arachidonic acid agonists (Misoprostol),
Histamine receptor antagonists (Ranitadine)
3. Protect mucosa from damage – Bismuth subcitrate / Sucralfate
4. Eradicate causiative agent (H.pylori) – Multi antibiotics
PPI + Clarithromycin +
Amoxycillin
PPI + Clarithromycin +
Metronidazole
PPI + Amoxycillin +
Metronidazole
PPI + Metronidazole +
Tetracycline + Bismuth
7 days > 90% success
7 days > 80% success
7 days 80-90% success
7 days 75% success
1st Line RX: Resistance to
Clarithromycin
1st Line RX: when Amox unsutible.
Metron has  resistance
1st Line RX: When Clariethro not
suitable
Complicate regimen, poorly tolerated.
Use only if 1st line fail
Week 8: Glycogen Storage Disease
Definition & Epidemiology
A disease resulting from a hereditary deficiency of one of the enzymes involved in the synthesis or
sequential degradation of glycogen. Depending on the tissue or organ distribution of the specific
enzyme in the normal state, glycogen storage in these disorders may be limited to a few tissues or be
more widespread.
Pathogenesis & Morphology
Based on pathophysiology, the disorders are broken into 2 groups:
1. Hepatic forms – The liver contains enzymes that synthesise glycogen for storage and ultimately
break it down into free glucose for release into blood. A deficenncy in hepatic enzymes
involved with gylcogen metabolism causing not only storage problems but also low BGL. Eg)
Von Gierk Dz (glucose-6-phosphatase deficiency - PBL).
2. Myopathic forms – in striated muscles glycogen is used as a source of energy. Energy is derived
from glycolysis with ultimately leads to the production of lactate. If enzymes that fuel the
glycolytic pathway are insufficient then glycogen storage occ within the muscles and causes
muscle weakness DT impaired energy production. Pts present with muscle cramps post exercise
and failure to  lactate levels with activity.
Treatment
Monitor BGL, Corn Starch??
Type
Affected
tissue
Liver glycogenoses
I (Von
Liver, intestine,
Gierke)
kidney
(25%)
Enzyme
defect
Clinical features
Tissue nec
for Dx
Outcome
Glucose-6phosphatase
Liver DNA
testing
III (Forbes)
(24%)
Liver, muscle
(abnormal
glycogen
structure)
Liver (abnormal
glycogen
structure)
Glycogen
debranching
enzyme
Hepatomegaly,
ketotic
hypoglycaemia,
stunted growth,
obesity, hypotonia
Like type I
Leucocytes,
liver,
muscle
Liver
Liver
phosphorylase
/phosphorylase
kinase
Phosphorylase
6 kinase
deficiency
Failure to thrive,
hepatomegaly,
cirrhosis and its
complications
Hepatomegaly with
hypoglycaemia in
childhood
If pts survive initial
hypoglycaemia,
prognosis is good;
hyperuricaemia is late
complication
Good prognosis but
progressive
neuropathy and
cardiomyopathy
Death in first 5 years
Liver transplantation
Liver
Good
Hepatomegaly,
hypoglycaemic
fatiguability
Liver,
muscle
No treatment
Heart failure,
cardiomyopathy
Fibroblasts,
muscles
Death in first 6
months
Muscle cramps and
myoglobinuria after
exercise (in adults)
muscles
Normal life-span; give
sucrose prior to
exercise
IV
(Anderson)
(3%)
VI (Hers)
(VI and
VIII =
30%)
VIII
Liver
Branching
enzyme
Leucocytes,
liver,
muscle
Muscle glycogenoses
II (Pompé)
(15%)
Liver,
muscle, heart
V (McArdle)
Muscle only
Lysosomal
acid αglucosidase
Phosphorylase
Week 9: Anorexia Nervosa
“You can never be too rich or too thin.” - Duchess of Windsor (1896-1986)
Epidemiology
AN is 10 times more common in females. The most common age of onset is 14-18 years, but AN has
been reported in girls as young as 8 years. It is believed to be more common in the SES.
Pathogenesis
- Socio-cultural factors are described as forming “the modern cult of thinness” in Western societies.
Evidence indicates a culture bound syndrome, as AN is rare in Asia and developing countries.
- Adverse life events my precipitate AN. Severe life events are found in the majority of patients with
onset after 25 years, and a minority of those with onset before 25 years.
- Personality disorder is found in at least 70% of those with AN. OCD most common.
Assessment and Presentation
The patient is usually a teenage female, brought in by her parents. There has been weight loss, cessation
of the menses, fine hair growth on the face and limbs, refusal to eat in the manner expected for her age
and family circumstances, particular avoidance of CHO and fatty foods, frequent weighing, often
vomiting and excessive laxative use, insomnia, irritability, sensitivity to cold, withdrawal from friends.
Anorexia Nervosa DSM-IV Diagnostic criteria
A. Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g.,
weight loss leading to maintenance of a body weight less than 85% of that expected)
B. Intense fear of gaining weight or becoming fat, even though underweight.
C. Distorted body image.
D. In postmenarche females, amenorrhea (the absence of at least three consecutive menstrual cycles).
Bulimia Nervosa DSM-IV Diagnostic criteria
A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both:
1. eating, in a discrete period of time and amount of food that is definitely larger than most people
would eat during the same time and in the same circumstances
2. a sense of lack of control over eating during the episode.
B. Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such as selfinduced vomiting; misuse of laxatives, diuretics, enemas, or other medications, fasting, or excessive
exercise.
C. The binge eating and inappropriate compensatory behaviour both occur, on average, at least twice a
week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of Anorexia nervosa.
Possible admission criteria (to be discussed with Adolescent Medicine consultant)
1. Physical ( for nasogastric resuscitation )
* Dehydration
* Postural hypotension (fall in systolic BP lying to standing > 20mmHg), bradycardia
* Hypothermia (temp. <35o C oral)
* Electrolyte abnormalities (eg. hypokalaemia, hypernatraemia)
* Severe weight loss (>30% of pre-morbid weight)
Investigations:
* Urea and electrolytes, creatinine
* Urinalysis - including pH (possibility of diuretic use )
* ECG (if K+ abnormal) A medical admission for resuscitation would usually result in a 4 week
period of inpatient treatment.
2. Psychiatric
Patients with anorexia nervosa may be at risk of suicide or other at-risk behavior (eg. acute bulimic
phase). These patients require urgent psychiatric assessment. On consultation with the adolescent
consultant and the adolescent psychiatry team, admission may be considered. The admission is usually
of shorter duration than if the patient were physically comprised.
Outcome
The annual mortality rate is 0.6%. Full recovery includes return to appropriate weight and continued
growth and development, restoration of menstruation, and normal eating behaviour and attitude with
regard to food and body shape.
Treatment
Inpatient treatment restores weight most rapidly (usually within three months).
There may be difficulty in persuading the patient to remain in an inpatient program.
Benefits include the omnipresence of skilled nursing staff, able to provide psychotherapy and
supervision. The patient is encouraged to take nutritious meals atregular meal times.
Family therapy is usually offered and is effective in helping to correct miscommunication and
misunderstandings within the family, and restore healthy eating habits (especially for pts < 19 years).
Drug treatment usually provides little benefit. Chlorpromazine or olanzapine may reduce distress and
stimulate the appetite. Antidepressants may be indicated for the treatment of major depression, but they
are ineffective in the presence of malnutrition.
Compulsory treatment and naso-gastric feeding depend on the provisions of local mental health
legislation. They are generally avoided as they are disruptive to the trusting patient-doctor relationship
and acceptance by the patient of responsibility for her actions. However, they become necessary should
malnutrition pose an immediate threat to life.
Follow-up
All patients with eating disorders require close and expert monitoring and long-term therapy. This
usually involves a combination of adolescent medicine and psychiatry out-patient support.