Download SAQ revision notes

SAQs_
 Elbow ossification centre- CRITOL
 Capitellum
 Radial head
 Internal (medial) epicondyle
 Trochlea
 Olecranon
 Lateral epicondyle
6/12 - 2yrs
4yrs
6yrs
8yrs
10yrs
12yrs
Osteosarcoma:
 M:F 1.5:1
 Most commonly affects adolescents
 peak incidence during period of maximum growth velocity
 2nd peak in >50yrs due to malignant change in Paget’s
 Primary is most often found at epiphysis or metaphysis of fastest growing sites – usually around
knee
 Patients with hereditary retinoblastoma have a 500X  risk of osteosarcoma
 ? related to deletions in long arm of chromosome 13
 Can also occur post radiotherapy
 Clinically
 43% femur, 19% tibia, 10% humerus
 pain or swelling initially noted
 Diagnosis
 plain XR/CXR/MRI/bone scan/biopsy
 CT thorax - 10-15% metastasize to the chest
 80-90% have micrometastases at presentation
 Poor prognostic factors
 age<10y
 large tumour >15cm
 osteoblastic cell type
 axial skeleton or humeral involvement
  serum LDH
 symptoms < 2/12
 metastases
NAI:
 XR features suggestive of NAI
 >1 #, especially if evolution of #s are different
 Subperiosteal bone formation
 never present on the day of the injury
 XR features pathognomic of NAI
 Metaphyseal long bone # - bucket handle (corner)
 Posterior rib #
 # pelvis/sternum/vertebral transverse processes
Unicameral Bone Cyst or Juvenile Bone Cysts:






Benign lesion which occurs during growth
20% of benign bone lesions
Age 5-15 years
Not found in adults
Sex male to female is 3:1
The most common location is the proximal humerus (67%) followed by the proximal femur
(15%)
 JBCs may be found in unusual sites (e.g. calcaneum, pelvis) in patients >17 years
Cysts may be Active or Latent: Active cysts are located near the growth plate, but they move further
away as the child grows and become inactive (latent)
 Presentation
 Asymptomatic
 Usually presents as a pathological fracture (~ 65%)
 Radiographic features
 Well defined, central osteolytic area with a thin sclerotic margin
 Metaphyseal in young - moves towards diaphysis with growth
 It fills and slightly expands the juxta- epiphyseal metaphysis
 CT not helpful unless the JBC is in the pelvis
 Treatment
 Treatment goal is to minimise fracture risk until the cyst heals (but this can take
years)
 Steroid injection
 1-3 percutaneous injections repeated at 2 monthly intervals
 60-80% success rate
 Curettage and bone graft - 50% recurrence rate and possibility of damage to the
growth plate
 Spontaneous healing after fracture occurs only in minority of cases
Epiphyseal injuries:
Risks:
 risk of premature fusion of the growth plate  limb shortening gait disturbance
 unequal growth may occur if only one part of the plate is injured
Ewing Sarcoma:
X-ray features of Ewing’s sarcoma:
Periosteal elevation, ‘onion-skin’ appearance, patchy lysis of marrow cavity, usually present in diaphysis
of long bones
 highly malignant
 Rare
 Arises from vascular endothelium in marrow
 Lower extremity > upper extremity
 Any long bone affected
 commonest metaphysis + diaphysis of femur, then humerus
 Occurs most commonly between 10 and 20yrs
 Whites >> blacks/asians
 M:F 3>2
 Clinically
 pain/ swelling/ erythema/wt loss/fatigue/fever
 Usual to have WCC, ESR,Hb at presn
 Radiologically: bone destruction with overlying ‘onion skin’ layers of periosteal new bone
 Usually lytic but can be sclerotic
 Investigations
 Biospy
 CT/MRI
 Bone scan
 Genetic screen
 Treatment
 pre-op chemotherapy
 vincristine/dactinomycin/cyclophosphamide
 Local resection
 Adjuvant chemo post-op -  recurrence
 Metastases - lungs/LN
 Poor prognosis associated with;
 Age, ESR, Leucocytosis, Serum LDH
 Prognosis
 if initial chemo/surgery unsuccessful - further chemo/radiotherapy gives 80-90% local
control
 without metastases at presentation:
40-70% long-term survival
Septic Arthritis:
 4 powerful predictors of septic arthritis
 WBC >12
 ESR >40
 Fever
 Non weight-bearing
 Combined sensitivity 99.6%
 Organisms identified:
 Staph. 58%,
 Pneumococcus 16%,
 Haem.Infl. 13%,
 Meningococcus. 8%,
 Strep. 5%
Koehler’s disease








Flattening, ↑ density and irregular shape of navicular of the foot
Osteochondrosis of navicular bone
Mean age 4-5,
boys:girls 6:1
15% bilateral
Aetiology: ?vasculitis / ? x-linked
Treatment: ? POP , recovery 3-15 months
Nutritional Rickets: x-ray
 Splayed, irregular epiphyses
 “Cupped” metaphyses
 “Hazy” growth plates
Blount’s deformity = tibia vara
 Varus knee, tibial bowing/proximal angulation
 Disturbed enchondral ossification of medial tibial plateau
 More common in black/Hispanic population
 Corrective surgery possible
 Associated with obesity
Scheuermann’s disease (adolescent kyphosis):




4-8% incidence on routine x-rays
Disorder of endplate growth
Document neurological/respiratory symptoms
Cobb’s angle
 > 40 degrees = brace
 > 70 degrees = surgery
Basal cell carcinoma
 Features:
rolled edge / pearly nodules/ keratin plug
 treatment options :
Excision Topical 5 fluorouracil ?DXT
Keratoacanthoma
 Umbilicated violaceous hyperkeratinous scaly
 treatment :
Observe, Biopsy , Excise Currette/Cauterise
A 10-year-old boy is brought to the department with bilateral parotid swelling. He has been diagnosed
as having mumps by his GP the previous day. He is otherwise well.
Give 3 complications of this condition (3)
 Orchitis
 Encephalitis
 Pancreatitis
Give 2 other causes of parotid swelling (2)
 Stone
 Cancer
 Alcohol abuse
 HIV
What 4 things are you going to do for this patient in A&E? (4)
 Notifiable disease
 Analgesia
 Feeding advice – non-acid foods
 Mouth care advice
 Vaccination advice
List 4 complications of an elbow fracture in any patient (4)
 Restricted movement
 Volkmann’s contracture
 Malunion
 Myositis ossificans
Diarrhoea in children:
List 4 things that you would ask for in the history. (4)
 Wet nappies
 Episodes of vomiting
 Frequency & description of stools and vomitus
 Affected contacts
 Food & Fluid intake (food poisoning- notifiable)
 Drugs taken
 Travel
 Other symptoms - abdominal pain, fever
 Weight loss- very important to assess degree of dehydration
What is the classification of dehydration according to APLS with percentages



Mild 5%
Moderate 5-10%
Severe >10%
Mild dehydration:
5%
 Decreased urine output (<4 wet nappies/24 hrs)
 Dry mouth
 Thirst
Moderate dehydration:
5 – 10%
 Sunken frontenelle in infants
 Sunken eyes
 Tachypnoea due to metabolic acidosis
 Tachycardia
Severe dehydration:
>10%
 Decreased skin turgor
 Drowsiness or irritability
Give 4 indications for admission in a child with gastroenteritis
 Moderate or severe dehydration (>10% dehydration needs i.v. fluid)
 Parents unable to cope at home
 High fever unresponsive to anti-pyretics
 Baby <3 months old
NB: severe illness with bloody diarrhoea, haemolysis and renal failure may result from infection with
vero-cytotoxin producing E. coli (E. coli VTEC O157)
CO poisoning may cause malaise and vomiting in several members of a family and be misdiagnosed as
food poisoning.
ABG in a patient with confusion and low blood glucosepH 7.3, pO2 >13kPa, pCO2 3kP, Base excess -6.0, Na 129, K 6.2, HCO3 12
What 2 urgent treatments Glucose
 i.v. hydrocortisone
Causes for hypoglycaemia: (ExPLAIN MAD)
 Exogenous- overdose of insulin or hypoglycaemic drugs
 Pituitary insufficiency & Post-gastric surgery
 Liver failure
 Adisonian crisis
 Insulinoma
 Non-pancreatic neoplasms
 Malaria
 Alcohol overdose
 Drugs
What are the criteria for ITU admission in asthma:







Life threatening features
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
Poor response to treatment
Erythema nodosum Causes:
i)
sarcoidosis
ii)
infections: streptococci, TB, infectious mononucleosis, chlamydia, viral
iii)
drugs: sulphonamides, OCP, salicylates
iv)
inflammatory bowel disease
v)
idiopathic
Management:
 Advise NSAID, bed rest, elevate legs.
 Remove underlying cause – OCP.
 Most attacks settle within 2-12 weeks.
 Systemic steroids may be used for severe cases.
Hyperkalaemia notes
Mild
(5.5-6.0)
Moderate
(6.1-6.9)
Severe (>7.0)
Causes
i)
ii)
iii)
iv)
v)
Factitious e.g. haemolysed sample.
Reduced renal excretion – ARF, CRF, K+ sparing diuretics e.g.
spironolactone.
Cell injury e.g. burns, rhabdomyolysis.
Hyperaldosteronism – Addison’s disease, drug induced (NSAID, ACE
inhibitors).
K+ cellular shifts – acidosis from any cause (DKA), drugs (suxamethonium).
Clinical features include muscle weakness/ cramps, paraesthesiae, hypotonia.
Treatment
i)
ii)
iii)
iv)
v)
vi)
10ml 10% calcium gluconate.
10u Actrapid with 50ml of 50% dextrose IV – helps cellular uptake of
Nebulised salbutamol.
Careful fluid balance, correct acidosis with sodium bicarbonate.
? calcium resonium.
Correct underlying cause.
K+.
Pulmonary embolism.
ECG: Sinus tachycardia is the most common ECG finding. RBBB and right axis deviation are usually
only present in large PE. There may be non-specific T wave changes in the anterior and inferior leads.
Investigations:
 Doppler USS of legs
 CTPA
 Inherited procoagulant screen (protein C, S, antithrombin III, Factor V Leiden)
 Autoimmune screen (anticardiolipin antibodies, ANA)
 USS or CT of abdomen and pelvis to look for occult masses
If a patient with suspected PE has arrested or is deteriorating, or in a stable patient with confirmed PE,
thrombolysis with alteplase 50mg IV is appropriate
The Wells score:







clinically suspected DVT - 3.0 points
alternative diagnosis is less likely than PE - 3.0 points
tachycardia - 1.5 points
immobilization/surgery in previous four weeks - 1.5 points
history of DVT or PE - 1.5 points
hemoptysis - 1.0 points
malignancy (treatment for within 6 months, palliative) - 1.0 points
Traditional interpretation



Score >6.0 - High (probability 59% based on pooled data[10])
Score 2.0 to 6.0 - Moderate (probability 29% based on pooled data[10])
Score <2.0 - Low (probability 15% based on pooled data[10])
Alternate interpretation (used practically)


Score > 4 - PE likely. Consider diagnostic imaging.
Score 4 or less - PE unlikely. Consider D-dimer to rule out PE.
Simplified Geneva Score









Age 65 years or over (1 point)
Previous DVT or PE (1 point)
General anesthesia or fracture within 1 month (1 point)
Active malignant condition or malignant condition that has been cured within 1 year (1 point)
Unilateral lower limb pain (1 point)
Hemoptysis (1 points)
Pain on deep palpation of lower limb and unilateral edema (1 point)
Heart rate of: 75 to 94 (1 point)
Heart rate of: Greater than 94 (1 point)
Patients with a score of 2 or less are considered unlikely to have a current PE. Authors suggest that the
likelihood of patients having a PE with a simplified Geneva score less than 2 and a normal D-Dimer is 3
percent.[6]
If signs of severe haemodynamic compromise, arrange for urgent CTPA or echocardiogram
 Collapse
 Hypotension
 A-a gradient more > x2 normal when CXR is normal and no other explanation
 Compromised peripheral perfusion
Request for CTPA / VQ scan should include
 Well’s score
 D-dimer level
 Previous lung disease (asthma, COPD) for which patient required admission or under care of
respiratory clinic
Oesophageal F.B.
Objects that stick in the oesophagus do so at sites of anatomical narrowing;






i)
ii)
iii)
Cricopharyngeus
Aortic indentation
Diaphragm
Neglected objects may result in oesophageal perforation and mediastinitis.
May require removal with rigid endoscopy. Foley catheters and magnets have also been used
but without much success.
TIMI score= Thrombolysis in Myocardial Infarction trials. (AMERICA)









i)
ii)
iii)
iv)
v)
vi)
vii)
Age ≥65 years
≥3 CAD risk factors
Prior CAD (stenosis >50%)
Aspirin in last 7 days
≥2 anginal events in ≤24 hours
ST deviation
Elevated cardiac markers
The score (0-7) gives the risk of cardiac events (death, MI or urgent revascularisation) within 14
days in TIMI IIB.
Typhoid:
Organism responsible – Salmonella typhi.
Spread by faecal/ oral route.
Along with malaria, first disease to consider if fever develops after visit to affected areas. Incubation
period 8-14 days.
Symptoms
1st phase - fever, headache, sweating, dry cough, myalgia, arthralgia, abdominal discomfort, anorexia,
constipation. Children are prone to diarrhoea. There may be splenomegaly.
‘Rose spots’ are pink macular spots on the lower chest or upper abdomen which blanch on pressure
2nd phase - fever, severe diarrhoea (may be bloody), unwell++, confusion.
Pneumonia and intestinal perforation are possible complications.
Treatment
Isolate and barrier nurse. Ciprofloxacin. Careful fluid balance. Notify communicable disease control.
3rd nerve palsy:



ptosis.
divergent strabismus and
pupil is dilated.
Differential diagnosis




Space occupying lesions,
after surgery (e.g. for pituitary lesions),
aneurysms of the posterior communicating artery,
Infections e.g. meningitis, encephalitis, herpes, syphilis.
Worthwhile mentioning;
Isolated 4th nerve palsy (superior oblique moves eye downward) → diplopia on downward gaze.
Isolated 6th nerve palsy (lateral rectus moves eye laterally) → failure of lateral movement with diplopia
on looking at the affected side.
Fascial spaces of the hand.
i)
Superficial pulp spaces of fingers
ii)
Synovial tendon sheaths of the flexor tendons ~ that of the 2nd, 3rd and 4th fingers are closed off
proximally at the metacarpal head but the
synovial sheaths of the thumb and little finger extend
into the palm (see
diagram).
iii)
Midpalmar space
iv)
Thenar space
Hand tendon injuries
 Flexor tendon injuries are often associated with neurovascular damage
 Extensor tendon injuries often associated with articular damage
Anatomy
Flexor tendons




Flexor tendons run a fibro-osseous canals
Synovial sheath for index to ring finger begins at neck of metacarpals
Synovial sheath of little finger is continuous with ulna bursa
Sheath thickened to form pulleys (A1 to A5)
Extensor tendons
 Extensor tendons are extra-synovial, except at the wrist
 Surrounded by extensive paratenon with segmental arterial input
 Extensor retinaculum prevents bowstringing of the extensors
 Main action is extension of the MCP joints
Zone of injury
Zone II is the ‘No Man’s Land’ where the flexor tendons are located in a narrow fibro-osseous
tunnel; injuries to the flexors in this region have a worse prognosis as the finger tends to
become stiff as adhesions form.
Flexor tendons
 Flexor tendons are divided into 5 zones
 Zone 1 is distal and Zone 5 is proximal
 The five zones are
o 1 - contains flexor digitorum profundus only distal to the insertion of
o
o
o
flexor digitorum superficialis
2 - from insertion of flexor digitorum superficialis to the proximal edge of
the A1 pulley
3 - from the proximal edge if the A1 pulley to the distal edge of the carpal
tunnel
4 - within the carpal tunnel
o
5 - proximal to the carpal tunnel
Extensor tendons
 Extensor tendons are divided into 8 zones
 Zones 1,3 and 5 lie over the DIP, PIP and MCP joints
Assessment







Accurate history required
Important to know handedness and patients occupation
Observing hand at rest my indicated tendons involved
Level of tendon injury may corresponds to site of any laceration - but not always
If both flexor tendons divided the finger will be extended
If profundus tendon alone divided then only the DIP will be extended
Further assessment should involve testing of individual tendons
o Flexor digitorum superficialis
o Flexor digitorum profundus
 Neurovascular assessment also required
Flexor tendon injuries






Early exploration and repair is required
Ideally surgery should be performed within 24 hours
Primary repair is the gold standard
Primary repair may not be possible id delayed presentation or tendons retracted
Antibiotic prophylaxis required if delayed presentation or would contamination
The ideal tendon repair requires
o Sutures easily placed in the tendon
o Secure suture knots
o Smooth junction if the tendon ends
o Minimal gapping at repair site
o Minimal interference with tendon vascularity
o Sufficient repair strength
 Many techniques of tendon repair have been described
 They invariably involve
o Core suture
o Epitendinous suture
Zone 1 injuries
 Direct repair usually possible
 Periosteal flap raised and tendon anchored with a core suture
Zone 2 to 5 injuries







Wounds should be excised and irrigated
May need to be extended to retrieve and repair tendons
Avoid incisions that cross skin creases
Careful planning required to prevent skin necrosis or contracture
Incision may be required in tendon sheaths between the main pulleys
Neurovascular bundles should be identified and repaired is necessary
Tendons should be repaired using a standard technique
Post-operative management
 After repair the hand should be placed in a back-slab with
o Wrist at 0 - 30 degrees
o MCP joints at 60 - 90 degrees
o PIP and DIP joints in full extension
 Hand should be elevated to reduce swelling
 Early mobilisation required to
o Reduce adhesion formation
o Improve tendon healing
o Improve final outcome
 Requires close supervision by hand physiotherapist
 Mobilisation can begin as early as first postoperative day
 Passive extension should be avoided
Extensor tendon injuries




Open exploration and repair is required
Can often be performed under local anaesthetic
Management depends on the zone of the injury
Proximal injuries require immobilisation with the wrist extended and the MCP joint
flexed
 Active movement can begin after 3 weeks
 Distal injuries require longer period of immobilisation
Anatomic Zones of the neck. (peneterating injuries)
Serving as the line of demarcation, the sternocleidomastoid separates the neck into anterior and
posterior triangles. The majority of the important vascular and visceral organs lie within the anterior
triangle bounded by the sternocleidomastoid posteriorly, the midline anteriorly, and the mandible
superiorly. Except for individual nerves to specific muscles, few vital structures cross the posterior
triangle, which is delineated by the sternocleidomastoid, the trapezius, and the clavicle (with the
exception of the region just superior to the clavicle).
For clinical purposes, the neck is partitioned into 3
Zone I, the base of the neck, is demarcated by the thoracic inlet inferiorly and the cricoid cartilage
superiorly. Structures at greatest risk in this zone are the great vessels (subclavian vessels,
brachiocephalic veins, common carotid arteries, aortic arch, and jugular veins, trachea, esophagus, lung
apices, cervical spine, spinal cord, and cervical nerve roots. Signs of a significant injury in the zone I
region may be hidden from inspection of the chest or the mediastinum.
Zone II encompasses the midportion of the neck and the region from the cricoid cartilage to the angle
of the mandible. Important structures in this region include the carotid and vertebral arteries, jugular
veins, pharynx, larynx, trachea, esophagus, and cervical spine and spinal cord. Zone II injuries are likely
to be the most apparent on inspection and tend not to be occult. Additionally, most carotid artery
injuries are associated with zone II injuries.
Zone III characterizes the superior aspect of the neck and is bounded by the angle of the mandible and
the base of the skull. Diverse structures, such as the salivary and parotid glands, esophagus, trachea,
vertebral bodies, carotid arteries, jugular veins, and major nerves (including cranial nerves IX-XII),
traverse this zone. Injuries in zone III can prove difficult to access surgically.
torsades de pointes
Also known as polymorphous ventricular tachycardia.
May present as recurrent syncope or dizziness.
Potentially reversible causes,
 hypokalaemia, hypocalcaemia, hypomagnesaemia,
 CHB,
 congenital long QT interval or
 drug related e.g. sotalol, tricyclics, antihistamines.
Torsades may be self-limiting but may progress to VF.
Treat by:
i)
Correcting underlying cause if possible.
ii)
IV magnesium sulphate 2g over 10 min.
iii)
May require temporary overdrive pacing.
subdural haematoma.
What groups of patients are prone to this?
 Alcoholics, the elderly, patients on anticoagulants.
List 5 features which may be present.
i)
ii)
iii)
iv)
v)
Headache
Fluctuating GCS
Confusion
Memory loss
Focal neurological deficit
Ulnar nerve palsy
Look for:
 Wasting of interossei: Wasting of the first dorsal interossei (ulnar n. supplies all interossei but
1st is almost always the first to become noticeably affected)
 ulnar claw appearance of hand. The claw hand appearance is due to paralysis of the intrinsic
hand muscles (lumbricals) which normally flex the MCPJs and extend the PIPJs. Unopposed
action of the long extensors pulls the MCPJs into hyperextension and the long flexors pull the
PIPJs into flexion.
 hypothenar wasting
 Scars/ deformity around elbow, wrist and hand.
 Trophic changes.
Motor:
Test flexor carpi ulnaris.
Test FDP in little finger.
Interossei: hold sheet of paper between ring and little fingers and withdraw.
First interosseus: attempt to adduct index against resistance, look and feel for contraction in 1st
webspace.
Froment’s test (adductor pollicis).
State 2 causes of this condition.


At wrist – lacerations, ganglia.
At elbow – occupational secondary to excessive leaning.
median nerve
Supplies:







Muscles in forearm (through anterior interosseous branch)
FPL
½ of FDP
FDS
FCR
Palmaris longus
Pronator quadratus and teres

Muscles in hand
lumbricals (lateral two)
opponens pollicis
abductor pollicis brevis
flexor pollicis brevis
L
O
A
F
Look for:

Index finger held in extension (Benediction attitude).



Motor:




Wasting of thenar muscles,
deformity/ scars around wrist and elbow.
Trophic changes.
Test APB by asking patient to lift thumb off flat surface against resistance.
Test FCR.
Test FPL and FDP in the index by flexing joint against resistance.
Test pronator quadratus by asking patient to pronate arm against resistance with elbow
extended.
Parkinson’s disease.
Name 3 features of this condition.
Tremor, rigidity, bradykinesia.
Other features: Stooped posture/ shuffling gait, fixed facial expression, speech problems, poor balance,
dementia
List 3 drugs used as treatment.
Levodopa, dopamine agonists (e.g. bromocriptine), selegiline
Causes for delirium:
H
I
D
D
E
N
M
A
P
hypoxia
infection
drugs
dural haemorrhage
endocrine (hypoglycaemia)
neoplasis / neurological
metabolic (hypercalcaemia)
alcohol (overdose, withdrawal, DT)
psychosis
Causes for increased anion gap
M
U
D
P
I
L
E
methanol
uraemia
DKA
INH
lactic acidosis
ethylene glycol
A 45 year old man is referred to the ED by his GP. He had a two day
history of progressive rightsided facial weakness and lower limb weakness. He had been previously fit apart from a mild URTI
one week previously.
Examination revealed a right-sided LMN CN VII palsy, generalised weakness of the legs with reflexes
diminished in the upper limbs and absent in the lower limbs. No other findings of note.
What is the diagnosis?
Guillan-Barré syndrome
What are the diagnostic features?
i)
Ascending, usually symmetrical, progressive LMN weakness.
ii)
Sensory loss is not usually profound but paraesthesiae may precede weakness. If there is a
sensory level then spinal cord compression should be the diagnosis until proved otherwise.
iii)
Reflexes are diminished.
iv)
Autonomic dysfunction is common.
v)
Ventilatory failure as disease progresses.
vi)
Often involves the cranial nerves (7th commonest).
How would you investigate this patient?
GBS is a diagnosis of exclusion with an extensive differential (see below). The management of the
patient with GBS is that of any patient with neuromuscular failure but specific measures include;
i)
Autonomic instability is a common feature so pulse/BP/ECG monitoring is essential.
ii)
Check spirometry and ABGs; early ventilatory support may be required
iii)
CT head if diagnosis unclear.
iv)
CSF analysis may be required – CSF protein characteristically rises and peaks at 4-6 weeks but
may be normal initially.
v)
Specific treatment with immunoglobulin.
What is the mortality of this condition?
Associated mortality is 10%.
Poor prognostic features on presentation:
 rapid onset,
 requirement for ventilation,
 age>40.
Grading system from I (able to run) to V (ventilated).
GBS probably represents an immune-mediated attack on peripheral nerves.
Differential diagnosis of acute generalized weakness:
Myasthenia gravis
Multiple sclerosis
Alcoholic myopathy
Poisoning (lead, organophosphates)
Tetanus
Spinal cord compression
Botulism
Hypokalaemia
Trifascicular block
This may show:
 1° heart block+RBBB+left anterior hemiblock
 1° heart block and LBBB
Block of the right bundle branch and either fascicle is bifascicular block. If this is combined with 1st
degree AV block then it is called trifascicular block.
If the patient is in CHB and bradyarrhythmia is causing severe haemodynamic compromise then
 Temporary pacing is the best option.
 Atropine 1mg IV bolus repeated if necessary up to 3mg.
 Isoprenaline 0.2mg IV if there is a delay in pacing and the patient remains unstable.
A 22 year old Caucasian woman presents acutely unwell. She has been previously fit and well and there
is no history of IV drug abuse. On examination she is pale, dyspnoeic and tachycardic rate 130, no
organomegaly.
Blood results show:
Hb
WCC
Plt
MCV
5.2
3.9
195
94
Bilirubin
ALT
AST
Alk phos
74
25
29
235
U+Es and clotting were normal. What is the diagnosis?
Haemolytic anaemia (normal MCV, elevated bilirubin).
Causes may be
 congenital (e.g. G-6-PD deficiency, sickle cell disease, hereditary spherocytosis) or
 acquired.
In this patient it is likely to be an acquired cause as hereditary disorders usually present early in life.
Splenomegaly would have suggested an underlying systemic disorder such as CLL or SLE.
Give 3 further investigations you would like to perform.
 Coomb’s test (detects circulating antibodies against RBC’s – presence may indicate autoimmune
or drug-induced haemolytic anaemia).
 Blood film
 CXR
Give 2 further features in the history that you would like to know.


Foreign travel
Drug history
Give some possible causes.
i)
Drugs e.g. penicillin, methyldopa.
ii)
Infections; viral, bacterial (mycoplasma) or protozoal (malaria).
iii)
Fava beans may precipitate haemolysis in patients with G-6PD deficiency.
iv)
Idiopathic autoimmune disorder.
v)
Underlying systemic disorder e.g. CLL, SLE.
A 72 year old lady is brought into the ED by concerned relatives. She has recently become increasingly
confused and agitated and today is very unwell. The only medication that she is taking is thyroxine. You
are concerned that she may be suffering a thyroid storm.
thyroid storm:
Look for evidence of thyroid disease e.g. goitre, exopthalmos.
It may be precipitated by
 Inappropriate cessation of anti-thyroid therapy,
 Infection,
 Trauma,
 DKA,
 Iodine administration,
 Recent surgery or
 Thyroid hormone overdose.
What other clinical signs would help confirm your diagnosis?
CVS



CNS



Other




Tachycardia, palpitations
AF
Cardiac failure
Agitation, anxiety
Tremor
Delirium, coma
Fever
Sweating
Abdominal pain
Vomiting
What would be your first investigation?
? TFTs
TFTs do not discriminate between simple thyrotoxicosis and thyroid crisis but an urgent TSH or free T4
may be useful if diagnosis is unclear.
What 3 medications would you use as first-line treatment?
1)
Steroids – hydrocortisone 200mg IV
2)
Propranolol 1mg IV inhibits peripheral T4→T3 conversion. Remember that a history of cardiac
failure (rate-dependent failure not included) or asthma may be CI for β-blockade; guanethidine may
also be used.
3)
Antithyroid drug; propylthiouracil is more effective than carbimazole.








Treat the precipitating factor if possible.
Fluid balance is important and CVP monitoring is usually necessary.
Monitor BM.
Sedation should be given if necessary.
Broad spectrum antibiotics are indicated if infection is suspected.
Do not give aspirin as this may displace thyroxine from thyroid binding globulin.
Treat fever with paracetamol.
Iodine will be given on the ITU once antithyroid medication has commenced effect.
Differential diagnosis
 neuroleptic malignant syndrome,
 septic shock,
 anticholinergic or sympathomimetic overdose,
 withdrawal states.
Another thyroid storm question was given:
A 35 year old woman is admitted confused, pyrexial and vomiting. Her flat-mate reports that she has
been unwell for the last three months and has lost weight. Three days previously she was bed-bound
with a severe cold. Her brother is diabetic.
On examination she is disorientated, pyrexial and tachycardic with an irregular pulse. There is no neck
stiffness and no focal neurological signs, no obvious focus of infection
Blood results were unremarkable, BM 5.2.
Clues in this question;
History
Weight loss
Recent viral illness
Family history of autoimmune disease (presumably she has Graves’ disease)
Examination
AF
Confusion
Pyrexial
A 35 year old male solicitor attends with a headache. He was
diagnosed as being hypertensive a year
ago and despite drug treatment including β-blockers, calcium antagonists and an ACE inhibitor his
blood pressure remains elevated. He drinks 4 pints of beer/day and smokes 2 cigars every evening. In
the department,
supine blood pressure is 210/110mmHg. Fundal examination shows
grade 3
retinopathy (flame haemorrhages and cotton wool exudates). The rest of the examination is normal.
Investigations:
Sodium 148, Potassium 3.0, Bicarbonate 32, Urea 4, Glucose
Urinalysis
NAD
What is the likely diagnosis?
4
Conn’s syndrome (primary hyperaldosteronism).
High aldosterone levels increase renal excretion of potassium, but this is not diagnostic for this disease.
Essential hypertension which is being treated with diuretics may mimic this.
High blood pressure is the main, and often only, symptom.
Excess secretion of aldosterone may be caused by an adrenal adenoma or adrenal hyperplasia.
What further investigations are indicated?
 CT abdomen.
 Serum aldosterone (elevated) and
 renin (low or undetectable).
However these are specialist investigations as they need to be done under controlled conditions. Refer
to an endocrinologist for appropriate treatment – surgical adrenalectomy (adenoma) or spironolactone
(hyperplasia).
Other conditions that may present with severe hypertension
 CVA,
 renal artery stenosis,
 CREST syndrome,
 renal failure,
 phaeochromocytoma,
 Cushing’s syndrome.
 Malignant hypertension
 Phaeochromocytomas
Phaeochromocytomas are catecholamine-producing tumours of the adrenal glands.
They may present with hypertension, hypertensive crises, cardiac arrhythmias, anxiety attacks, tremor,
sweating and cold extremities. Careful rehydration is necessary before α-blockade and referral.
Send urinary and plasma catecholamines.
Malignant hypertension may presents with hypertensive encephalopathy (headache, nausea, vomiting,
visual symptoms, confusion, fits) and needs careful blood pressure management after consultation with
physicians.
Cautious reduction of the BP is necessary to avoid complication such as CVA and AMI
Avoid sublingual nifedipine.
A 64 year old Somali woman has a 6 month history of significant weight loss and episodic colicky
abdominal pain not associated with meals or posture and no change in bowel habit.
Investigations:
Sodium 125, Potassium 6.0, Urea
14, Calcium
2.76
(2.2-2.6), Glucose
3.3
What is the diagnosis?
Addison’s disease.
This frequently has an insidious onset with weakness, apathy and anorexia in addition to the other
symptoms described.
80% of cases in the UK are idiopathic (autoimmune);
Other causes include TB, metastatic disease, drugs (e.g. rifampicin, phenytoin), adrenal haemorrhage 2°
anticoagulation and sepsis.
The biochemical picture is typical.
Treatment consists of identifying the underlying cause and steroid replacement therapy.
Chronic features of Addison’s disease include areas of vitiligo and hyperpigmentation in the palmar
creases, buccal mucosae and axillae.
Addisonian crisis (acute adrenal cortical insufficiency) is rare and usually precipitated by sudden steroid
withdrawal.
Other causes include trauma, infection or stress.
Main features are shock, confusion and hypoglycaemia.
Treatment of crisis involves
i)
ii)
iii)
iv)
v)
Fluid resuscitation
Check BM and treat if hypoglycaemic
Take blood for cortisol and ACTH
Hydrocortisone 100mg IV
Infection screen and IVAB if suspected infection
Q.
A 45 year old smoker complains of tiredness and weakness.
Investigations:
Blood pressure 180/110mmHg
Sodium 140, Potassium 2.8, Bicarbonate 32, Urea 5, Glucose 12
What is the probable diagnosis?
ACTH-producing oat cell lung carcinoma
Cushing’s syndrome, caused by excess glucocorticoids.
The commonest cause is the use of steroid medications e.g. for asthma.
Classical signs and symptoms;
 Moon face
 Central obesity
 Abdominal striae & Thinning skin
 Weight gain
 Osteoporosis
 Diabetes
 Hypertension
 Infections esp. skin
What investigations would you perform to confirm your diagnosis?



CXR
Serum and urine cortisol
Dexamethasone suppression test
Pretibial myxoedema.
Can be present in either Graves’ disease or hypothyroidism.
It is an infiltrative dermopathy that most frequently appears symmetrically over the anterior tibia and
dorsum of feet.
Can present in nodular or diffuse forms.
It is likely that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and
collagen by dermal fibroblasts.
Treatment with steroids and/or immunoglobulins may give some relief.
This patient presented with a rash following an URTI.
What is the likely diagnosis?
Henoch-Schonlein purpura.
Aetiology
IgA-mediated vasculitis of small blood vessels. The exact causative mechanism is unknown but it usually
follows bacterial (particularly strep.) or viral infection.
What is the likely sex and age of the patient?
M:F
2:1
4-11 years
What is the prognosis?
Generally good but need follow up because of the possibility of delayed renal involvement and
development of nephrotic syndrome which indicates severe disease.
What other symptoms may the patient present with?
i)
ii)
iii)
iv)
v)
vi)
Malaise, low grade fever
Hepatosplenomegaly
Lymphadenopathy
Colicky abdominal pain (may develop bloody diarrhoea, intussusception).
Arthritis/ arthralgia
Testicular pain and/ or swelling
Causes of purpuric rashes in children:
i)
ii)
iii)
iv)
meningococcaemia
HSP
thrombocytopenia 2° ITP, leukaemia, aplastic anaemia
trauma, coughing or retching
Erythema multiforme:
Typical target lesions. It can occur at any age
This is a localised form of vasculitis.
Causes:
 idiopathic,
 drugs (e.g. sulphonamides, phenytoin, barbiturates),
 infection (viral (esp. Herpes simplex) or Mycoplasma pneumonia), or
 related to malignancy.
What is the eponymous name for the severe form of this condition?
Stevens-Johnson syndrome. There may be oral, ocular and genital lesions. This form carries a significant
morbidity and mortality;
complications may include renal and respiratory involvement.
Management is symptomatic. Steroids may reduce the severity of the attack. The underlying cause
should be treated where possible.
SLE.
This is a chronic autoimmune disorder characterised by the production of a range of autoantibodies,
most commonly ANA. Commoner in young women.
Patients may present as a new diagnosis or with a flare up of the disease.
Clinical features (in descending order of frequency);
Constitutional
Musculoskeletal
Cutaneous
Haematological
Neuropsychiatric
Renal
CVS or RS
Apthous ulcers
fever, malaise, weight loss
athralgia, myalgia
butterfly rash, photosensitive rash, discoid lupus, Raynaud’s
thrombocytopenia, anaemia, leucopenia
depression, psychosis, fits, CN lesions, ataxia
glomerulonephritis, nephritic syndrome
pleurisy, pericarditis, pericardial/ pleural effusions
What 4 important emergency investigations would you now consider?
FBC, U&E, CRP, CXR, urinalysis, ECG
Other investigations include ANA, DNA, ENA, ACA, complement levels, viral serology, 24hr urine
collection.
80% of patients are ANA +ve. Pneumococcal and meningococcal infections are more common in patients
with SLE as a consequence of deficiencies of the complement pathway.
Treatment is with steroids, immunosuppresants e.g. azathioprine, antibiotics if infection suspected.
Lung abscess and Empyema:
The most common cause of lung abscess, or empyema (pus in the pleural cavity), is aspiration. Patients
at risk include the elderly, alcoholics, those with poor dentition or primary lung disease. Other causes of
empyema include penetrating chest trauma (including chest drains) and oesophageal rupture.
The patient is usually elderly and the abscess is most commonly located in the dependent part of the
lung on the right side. Organisms are usually polymicrobial oral flora e.g. Bacteroides and
Fusobacterium.
Increasingly in the paediatric population S. aureus has become the predominant organism because of
the use of the pneumococcal conjugate vaccine.
Treatment is with broad-spectrum antibiotics and drainage by tube thoracostomy.
Primary chancre of syphilis.
What is the offending organism and how is it transmitted?
Treponema pallidum, a spirochaete.
 It is almost always transmitted by sexual contact with infectious lesions
 Can be transmitted in utero and by blood transfusion.
List 4 other causes of genital ulceration.
i)
ii)
iii)
iv)
Other infections e.g. herpes simplex, gonorrhoea.
Neoplasms e.g. carcinoma of penis
Behçet’s disease.
Trauma (may be self-inflicted).
What investigations could confirm the diagnosis?
Direct visualisation by darkfield microscopy.
VDRL serology.
What is the treatment of choice?
Primary and secondary syphilis are highly responsive to penicillin and cure is likely.
How may secondary syphilis present?




localised or diffuse mucocutaneous rash and
generalised lymphadenopathy.
Constitutional symptoms include malaise, sore throat, headache, fever, arthralgia and myalgia.
Other less common manifestations include hepatitis, nephropathy, optic neuritis, proctitis.
Necrobiosis lipoidica.

Commonly affects the shins, seen more often in women. More than fifty percent of sufferers have
DM. It is a chronic condition; ulceration may occur.
 Flare-ups may respond to cortisone cream or UV light. Aspirin may also help.
Pancreatitis
Aetiologies (GET SMASHED)
Gall stone, Ethanol, trauma & post-surgery (ERCP), steroid, mumps, autoimmune (SLE),
hyperlipidaemia/hypercalcaemia, scorpion bite, drugs (salicylate)
USG should be organized within 24 hours to find out the cause.
CT scan is indicated
 To confirm the diagnosis of acute necotising pancreatitis
 If patient deteriorates - to confirm the diagnosis of necrosis and CT guided aspiration of the
infected secretion.
Antibiotics is required in
 Pancreatic necrosis
 Biliary tract obstruction
 Cephalosporine or carbapenum
Complications
Local
 Necrosis ± infection.
 Fluid collections.
 Pseudocysts.
 GI haemorrhage.
Systemic
 Shock.
 Coagulopathy & DIC
 Renal failure.
 Respiratory failure & ARDS
 Hyperglycaemia.
 Hypocalcaemia.
Glasgow criteria
Glasgow's criteria[: The original system used 9 data elements. This was subsequently modified to 8 data
elements, with removal of assessment for transaminase levels (either AST (SGOT) or ALT (SGPT) greater
than 100 U/L).
On Admission
1.
2.
3.
4.
5.
Age >55 yrs
WBC Count >16 x109/L
Blood Glucose >10 mmol/L (No Diabetic History)
Serum Urea >16 mmol/L ( No response to IV fluids)
Arterial Oxygen Saturation <7.9 kPa
Within 48 hours
1.
2.
3.
4.
Serum Calcium <2 mmol/L
Serum Albumin <32 g/L
LDH >600 units/L
AST/ALT >100 units/L
All patients with Glasgow score 3 or more should be referred to ITU / HDU.
Orbital Cellulitis:
Name 2 possible causative organisms.
Since invasive H. influenza infection has been all but eradicated by immunisation, S. aureus and Strep.
pneumoniae are the commonest pathogens.
What is the likely source of infection?
It is usually caused by spread from the sinuses (ethmoidal or para-nasal) but may arise from local trauma
(e.g. bites, foreign body) or haematological spread.
List 3 complications.
i) Cavernous sinus thrombosis.
ii) Cerebral abscess.
iii) Optic nerve compression leading to loss of vision.
Patients should be admitted under joint care of paeds./ ENT/ eyes.
Antibiotics – IV flucloxacillin and metronidazole.
Essential investigation is CT scan of orbit and sinuses.
Community Acquired Pneumonia:
Investigations:
 All patients admitted to hospital: FBC, U&E, CRP, ABG, blood cultures, sputum cultures.
 For patients with severe CAP: pneumococcal antigen, legionella urine antigen, chlamydial
antigen and mycoplasma CFT are appropriate.
What features may indicate an adverse prognosis?
Core clinical adverse features (CURB 65)





Confusion:
new confusion or defined as an AMT score of 8 or less.
Urea:
raised >7mmol/l.
Respiratory rate:
raised ≥30/min.
Blood pressure: low BP systolic <90 and or diastolic ≤60.
Age:
>65 years.
A score of 2 or greater on CURB 65 means hospital treatment is usually necessary.
Pre-existing
 Age >50 years.
 Presence of co-existing disease.
Additional adverse features
 Hypoxaemia: SaO2 <92% or PaO2 <8kPa regardless of FiO2.

Bilateral or multilobe involvement on the CXR.
What antibiotic therapy is recommended?


For hospital-treated, not severe CAP: amoxicillin 500mg tds plus clarithromycin 500mg bd.
For severe CAP: co-amoxiclav 1.2g tds IV plus clarithromycin 500mg bd.
BTS guideline recommends macrolide antibiotics In children above the age of 5 years, but macrolide
antibiotics smay be preferred preferred in children because it is effective against pneumococci as well as
pertusis and mycoplasma, whereas amoxicillin is not effective against pertusis and mycoplasma.
Infectious endocarditis. Mitral valve is most commonly affected.
Presentation:
malaise, night sweats and weight loss
What signs will you look for on further examination?
i)
ii)
iii)
iv)
v)
vi)
vii)
Viii
Splenomegaly.
Roth spots (retinal haemorrhages with central clearing).
Splinter haemorrhages.
Anaemia.
Janeway lesions (red skin spots on the palms and soles).
Osler’s nodes (red, painful intradermal pads in the fingers and toes).
Urine- microscopic Haematuria.
Changing murmur
What investigations are appropriate?
ECG, CXR, FBC, blood cultures X 3, ECHO, ASO test.
Organisms:
 Commonest organism is S. viridans (found in the mouth, 40%)
 others
o S. aureus (which presents with heart failure),
o enterococci and
o fungal e.g. candida, aspergillus.
Complications
 valve destruction,
 heart block,
 LVF,
 embolic events,
 lung abscesses (right-sided disease).
Which patients are at risk from this condition?
May develop on previously normal valves as well as diseased valves or prosthetic valves.
IV drug abusers are prone to staphyloccal infection of the tricuspid valve (i.e. right-sided), with fever and
pneumonia from septic PE.
What antibiotics would be appropriate for initial management?
Benzylpenicillin and gentamicin IV.
Hypertrophic Pyloric stenosis.
Hypochloraemic, hypokalaemic alkalosis.
Congenital pyloric stenosis is the most common cause of intestinal obstruction in infancy. It is more
prevalent in males, usually a first-born aged 3-6 months. Vomiting is projectile and bile-free. Test feed
may reveal a palpable tumour. USS may also be used in diagnosis.
Vomiting leads to the characteristic metabolic picture as the metabolic alkalosis leads to K+ loss in the
urine.
The child should be kept NBM and an NG tube passed. If rehydration is necessary use ½ Normal saline
with dextrose. Refer for surgery – Ramstedt’s pyloromyotomy.
Pyloric stenosis in adults results from scarring, usually secondary to a chronic DU. It presents with
vomiting, dehydration, weight loss and malnutrition. There may be an audible succession splash.
HIV .
RNA retrovirus. Binds to CD4 receptors on T-lymphocytes, monocytes and macrophages. These CD4 cells
normally play a crucial role in co-ordinating the immune response. CD4 cell counts provide an indication
of disease progression.
Presentations to the ED:
i)
Respiratory: PCP pneumonia, pulmonary TB, Aspergillus, Cryptococcus.
ii)
Neurological: Cryptococcus meningitis, cerebral toxoplasmosis, cerebral
encephalitis.
iii)
Eye:
lymphoma,
CMV
CMV retinitis.
iv)
GI problems: Nausea, vomiting, weight loss are common and may be drug
effects.
Oesophageal candida or herpes simplex infection.
CMV colitis and other causes of infectious diarrhoea e.g. cryptosporidium,
Giardia, Salmonella.
v)
Mucocutaneous:
Oral candidiasis, seborrheic dermatisis. Oral hairy
herpes infections, molluscum contagiosum, Kaposi’s
sarcoma.
leukoplakia,
Explain the mechanism for these deformities.
Mallet:
avulsion fracture at dorsal aspect of base of terminal phalanx or
terminal portion of extensor tendon.
Boutonniere: rupture or laceration of central slip of extensor tendon, remaining
parts of extensor tendon slip along side of finger
producing
deformity.
Swan neck:
damage to volar plate of the PIP joint either by trauma or
degeneration as in RA.
avulsion
of
lateral
characteristic
Inability to extend thumb:
Rupture of EPL may occur a few weeks after (usually undisplaced)
fracture of the distal radius. Tendon ruptures are also associated with RA, OA, CRF and SLE.
i)
Ankylosing spondylitis.
Usually presents as chronic low back pain in men aged 15-30. There is progressive spinal fusion and
immobility. Other features include iritis, apical lung fibrosis and plantar fasciitis. There may be a
normochromic anaemia and ↑ ESR. X-ray shows bamboo spine, obliterated SI joints.
ii)
Reiter’s syndrome.
Triad of urethritis, conjunctivitis and seronegative arthritis. May cause monoarthritis, typically of larger
lower limb joint. Other features include psoriaform skin lesions (keratoderma blenorrhagicum), circinate
balanitis and plantar fasciitis. May progress to give aortic incompetence, heart block, pericarditis.
iii)
Behcet’s syndrome.
Polyarthritis (± erythema nodosum) with painful orogenital ulceration and iritis.
iv)
Felty’s syndrome.
A variant of RA characterised by RA, splenomegaly, leucopenia and recurrent infections. Splenectomy
may improve the WCC.
Necrotising fasciitis
Group A haemolytic Strep. pyogenes, may also be Staph. aureus and
anaerobes.
Gas gangrene
Clostridium perfringens (anaerobic Gram +ve bacillus, produces exotoxins).
Treatment involves analgesia, resuscitation, IV antibiotics (penicillin with metronidazole), surgical
debridement of affected tissues. Sometimes hyperbaric oxygen is used and gas gangrene antitoxin may
be useful if Clostridium is suspected.
Q
A 45 year old woman with a long-standing history of RA presents with a 6-month history of
worsening dyspnoea. She does not experience orthopnea. No raised JVP, heart sounds normal. ECG is
normal. Blood gases on air show type 1 respiratory failure, no acidosis.
What is the probable diagnosis?
Pulmonary fibrosis 2° to RA.
Other extra-articular features may include SC nodules, vasculitis, splenomegaly, neuropathy, anaemia,
pleurisy, pericarditis and eye problems.
What other physical signs would you look for?
RA is a symmetrical polyarthritis typically affecting the hands and feet of young women. Remember
cervical-spine involvement.
X-rays show soft tissue swelling, peri-articular erosions and joint space narrowing, deformities
She should undergo CXR, ? CT chest and spirometry.
5)
A 65 year old woman presents c/o severe headaches for several weeks and of now having lost
vision in one eye. The eye is not red or painful.
Investigations show FBC normal, ESR 90.
What is the probable diagnosis?
Temporal arteritis.
Beware in any patient >50yrs who presents with new headache or change in headache, weight loss,
night sweats and jaw claudication.
There is an association with polymyalgia.
What features would be important in the physical examination?
i)
Tenderness over temporal artery or loss of pulsation.
ii)
fundoscopy – papilloedema may occur late in the disease.
iii)
if the patient is in AF or has a carotid bruit then need to consider other causes of painless
monocular visual loss, e.g. central retinal artery occlusion, stroke.
What diagnostic test will confirm this diagnosis and what treatment is indicated in the ED?
Temporal artery biopsy. Hydrocortisone 200mg IV.
What may be the Side Effects of steroids in the elderly?
Loss of diabetic control, peptic ulceration, hypertension, thinning of skin (bruise easily), osteoporosis.
rness over temporal artery or loss of pulsation.
Causes of a prolonged QT interval.
i)
Hereditary
 Lange-Nielsen (high-tone deafness) and
 Romano-Ward syndromes).
Both carry risk of ventricular arrhythmias and are associated with torsades de pointes and sudden
cardiac death.
ii)
Hypocalcaemia: clinical features include paraesthesiae, tetany, fits and psychiatric disturbance.
Look for Trousseau’s sign (carpal spasm when brachial artery occluded with BP cuff) and Chvostek’s sign
(twitching of facial muscles when tapping facial nerve) and papilloedema.
iii)
Drugs: anti-arrhythmics (quinidine, amiodarone, sotalol), antihistamines,
organophosphates.
iv)
Hypomagnesaemia
v)
Hypokalaemia
vi)
Intrinsic heart disease (IHD, myocarditis).
vii)
SAH
viii)
Hypothermia
antimalarials,
Congenital long QT syndromes may be treated with long-term propranolol or an ICD. Other family
members should be screened for disease.
infectious diseases of childhood.
Pertussis
Bordetella pertussis. Notifiable disease. Incubation 5-14 days.
Features ~ coryza wirth worsening cough, may persist for weeks. Risk of apnoeic episodes in infants.
Treat with erythromycin.
Measles
Viral infection, droplet spread. Incubation 10-14 days.
Features ~ fever, malaise, coryza, conjunctivitis, cough. Koplik’s spots. Spreading maculopapular rash.
Treatment is symptomatic unless complications ensue e.g. otitis media, bacterial pneumonia,
encephalitis. Mortality low in UK.
Mumps
Viral infection, saliva and droplet spread. Incubation 14-18 days.
Features ~ fever, pain and swelling of parotids, orchitis (10%). Aseptic meningitis may occur. Treament is
with analgesia and possibly steroids for orchitis.
Rubella
Viral infection, airborne spread. Incubation 2-3 weeks.
Usually a mild disease with rash, mild fever, occipital lymphadenopathy and arthralgia. Infection during
pregnancy may cause severe congenital disorders. If any concern take blood for viral antibody levels.
TORCH agents
 Toxoplasmosis may cause periventricular microglial nodules, thrombosis and necrosis;
obstruction of cerebral foramina causes hydrocephalus; with prolonged survival, there is
intracranial calcification, hepatocellular, adrenal, pulmonary, cardiac necrosis and
extramedullary hematopoiesis
 Rubella may cause LBW, hepatosplenomegaly, petechiae and purpura, congenital heart disease,
cataracts, microophthalmia and microcephaly; CNS symptoms include lethargy, irritability,
dystonia, bulging fontanelles and seizures..
 Cytomegalovirus may cause hepatosplenomegaly, hyperbilirubinemia, neonatal
thrombocytopenia, microcephaly and a mortality of 20-30%; later manifestations include mental
retardation, deafness, psychomotor delays, dysodontogenesis, chorioretinitis, learning
disabilities; ± 33 000 congenital cases/year–US, of which 10% are symptomatic
 Herpes simplex may cause prematurity, and becomes symptomatic after the first week of life;
CNS symptoms include irritability, seizures, chorioretinitis, hydrocephalus, flaccid or spastic
paralysis, opisthotonos, decerebrate rigidity and coma; in neonatal HSV infection, no deaths
occur in those with localized disease, 15% die if encephalitis is present and 57% die if HSV is
disseminated, potentially evoking DIC NEJM 1991; 324:450
 Syphilis–an optional 'TORCH' Congenital syphilis has ↑ to epidemic rates in the urban US since
the mid-1980s; the clinical findings are nonspecific and include fever, lethargy, failure to thrive,
and irritability
TORCH panel
TORCH antibody panel Pediatrics A serologic screen for diagnosing prenatal infection; the finding of ↑
IgM in the neonate implies in utero infection by one of the TORCH agents–toxoplasma, rubella, CMV,
herpes simplex, which is then characterized by measuring specific IgM levels.
A 25 year old man attends after returning from a diving holiday that
headache, lower back pain and painful (nontender) knees.
day. He complains of mild
Give 4 important points in the history.
i)
Time of onset of Sx related to the dive.
ii)
Dive profile (depth, duration, activity, speed of ascent, water temp. etc).
iii)
Previous medical history.
iv)
Did he fly back? (decompression illness may be precipitated if
diving and flying).
insufficient time is left between
If suspected, discuss with Duty Diving Doctor. Treatment is recompression, pending this give high-flow
O2, IV fluids and aspirin (to prevent sludging).
Meningitis:
What organisms are responsible and what is appropriate initial management?
Meningitis may be bacterial, viral or rarely, fungal. Usual bacteria are Neisseria meningitidis or
pneumococcus. Other bacteria (e.g. TB, Listeria) may cause meningitis in the elderly, the
immunosuppressed and neonates.
Initial management consists of A/B/C and:
i)
cefotaxime or ceftriaxone 80mg/kg.
ii)
look for signs of shock or raised ICP (decreasing or fluctuating level of consciousness, unequal
or poorly reacting pupils, focal neurological
signs, abnormal posturing or seizures).
iii)
if shocked give colloid bolus (20ml/kg 4.5% HAS) and repeat if necessary; observe closely, may
require inotropes, intubation etc. on
PICU.
iv)
if evidence of ↑ ICP, give mannitol (0.25g/kg bolus) followed by frusemide
(1mg/kg)
and
steroids (dexamethasone 0.4mg/kg bd). Treat seizures as usual.
Will require intubation and PICU.
What risks are there to healthcare workers?
Minimal; prophylaxis is unnecessary unless mouth-to-mouth resuscitation has occurred. Household
contacts should be given rifampicin (warn about orange discoloration of urine and interaction with OCP).
Remember to inform the Public Health Department.
Hydrofluoric acid.
HF acid rapidly crosses lipid membranes and penetrates tissues deeply where it releases the highly toxic
fluoride ion. These ions may gain access to the circulation producing a variety of systemic problems,
notably hypocalcaemia.
What is the immediate management?
i)
ii)
iii)
iv)
v)
Analgesia.
Copious lavage.
Calcium gluconate gel may be applied to the burn.
Check serum Ca2+, U&E and Mg2+.
Record ECG and monitor.
vi)
Treat hypocalcaemia.
Swallowed button battery
What is the appropriate course of action?
NPIS advice:
i)
Batteries lodged in the oesophagus require immediate retrieval by
endoscopy.
ii)
Batteries in the stomach require review at 48 hours to ensure that they have passed through
the pylorus; if not then they require endoscopic removal.
ii)
If the battery has passed through the pylorus and remains
asymptomatic
then
stools
should be monitored for up to one week and the patient reviewed if the battery has not passed.
iv)
If at any time the patient develops symptoms or signs of GI bleeding or obstruction then the
battery should be retrieved.
Human bite- treatment:
i)
Analgesia.
ii)
History regarding tetanus status.
iii)
X-ray.
iv)
Wound irrigation/ exploration.
v)
Augmentin.
vi)
Counsel regarding HIV and hep. B transmission: if thought to be highprophylaxis.
DVT:
Wells score
1)
2)
3)
4)
5)
6)
7)
8)
9)
active cancer (treatment ongoing or within 6 months of palliative)
paralysis, paresis or immobilisation of lower limb
recently bedridden >3 days or major surgery within 4 weeks
localised tenderness along the deep veins
entire leg swollen
calf swelling 3cm more than asymptomatic side
pitting oedema confined to affected leg
dilated superficial veins
alternative diagnosis as likely or greater than DVT
Wells categorized patients into;
Low risk
(score ≤0)
Moderate risk (score 1 or 2)
High risk
(score ≥3)
risk
then
1
1
1
1
1
1
1
1
-2
give
The use of the Wells score is as a ‘rule out’ test in combination with D-dimer testing; i.e. those patients
who have a low risk and a -ve D-dimer do not require further investigation for DVT. Anyone with a
moderate risk should undergo duplex USS.
Amaurosis fugax
Artery involved:
left internal carotid.
Other features of carotid TIA may be hemiparesis or dysphasia.
Most TIAs result from thrombo-embolic disease involving either the heart or extra-cranial vessels.
Differential diagnosis includes cerebral tumour, focal migraine, Todd’s paresis, hypoglycaemic episode
and other causes of monocular visual loss e.g. retinal vessel occlusion, temporal arteritis, vitreous
haemorrhage etc.
Ask about risk factors e.g. hypertension, polycythaemia, anaemia, vascultits, sickle cell disease. Look for
AF, heart murmurs (mitral stenosis, artificial valves), carotid bruit, evidence of AMI.
Check BM, send bloods and get ECG and CXR.
Acute uveitis.
The pupil is irregular due to previous adhesions.
Give 5 associated diseases.
Ankylosing spondylitis, ulcerative colitis, sarcoid, AIDS, Behcet’s syndrome.
Outline your management plan.
Give analgesia.
Check VA.
Pain on accommodation as pupils react is called Talbot’s test.
Fundoscopy,
Slit lamp examination.
Refer to ophthalmology for steroid eye drops.
Antidiuretic Hormone (ADH) is produced in response to serious illness, pain, dehydration, in
response to surgery (see Box B) ADH leads to reduced urine output, concentrated urine and
retention of ‘water’ and can result in hyponatraemia. Maintenance fluid requirements in illness
are therefore LESS than maintenance fluid requirements in health. Maintenance fluids in illness
should be restricted to 2/3rds (66%) of calculated requirements
Child at risk of hyponatraemia
Na+ <135mmol/L
Peri or post-operative
CNS infection
Head injury
Excess gastric or GI losses
Bronchiolitis
Severe sepsis
Hypotension
Intravascular volume depletion
Gastroenteritis with dehydration
Salt-wasting syndromes
Estimate deficit in Dehydration: mL = %dehydration x weight (kg) x 10
Give 0.9% sodium chloride (+/- glucose +/- potassium) Replace over 24 hours (or 48 hours if Na+
<135mmol/L or >145mmol/L)
Fluid volumes in dehydration
 Calculate deficit to be replaced over 24hours (or 48 hrs if hypo/hypernatraemia)
 Add to this maintenance fluid requirement in 24 hours (full / 100% maintenance)
 Add to this ongoing losses
Losses should be replaced mL for mL with a solution roughly comparable to this loss
e.g. NG loss with 0.9% sodium chloride with 10mmol KCl per 500mL.
Fluid volumes without dehydration
 The majority of children requiring IV fluids are sick and will be ‘fluid retaining’ under the
influence of ADH (Box B). In this case, fluids should be restricted to 2/3rds (66%) of
maintenance volumes.
 In a well child (eg. pre-op and NBM) full maintenance can be given.
Fluid Type
 In those at risk of ADH secretion (Box B):
o Sodium chloride 0.9% (with glucose 5% in infants under 1 year and consider
glucose requirement in older children)
o OR Compound sodium lactate (Hartmann’s solution) with / without 1% glucose
 In other patients, or in response to U&E results:
o Sodium Chloride 0.45% with 2.5% or 5% glucose
Potassium replacement
 Potassium requirements are approx 2mmol/kg/day. Once the plasma potassium is
known, and child has passed urine, 500mL bags with 10mmol KCl pre-added should be
used. If potassium is low, 20mmol/500mL is used. Higher concentrations may be used at
the discretion of the consultant (consider cardiac monitoring/ central line insertion).
Pharmacy stock sodium chloride 0.9% with 60mmol/litre, 80mmol/litre or
40mmol/500mL.
Hypoglycaemia - Glucose <3mmol/L.
 Medical emergency - Give 5mL/kg of glucose 10%. Recheck level after 15 mins. Review
maintenance fluids. Monitor.
Symptomatic hyponatraemia in children:
 Check U&E (Ca and Mg) if symptoms of nausea, vomiting, headache, irritability, altered
consciousness, seizures or apnoea.
If Na <130mmol/L get senior advice immediately. If child is seizing, commence infusion
of sodium chloride 3% solution. One mL/Kg of sodium chloride 3% will normally raise the
serum sodium by 1mmol/L. Serum Na should be raised quickly until the child has
regained consciousness and has stopped fitting or the serum Na is above 125mmol/L.
The amount of Na required can be calculated according to the following formula:
o mmol of Na required = (130-present serum Na) x 0.6 x Weight (kg)
o sodium chloride 3% is made by withdrawing 5mL of sodium chloride 30%
(available on NICU) and making it up to 50mL with water for
injections.immediately prior to administration
Asymptomatic hyponatraemia with normovolaemia
 Fluid restrict to 50% maintenance
 If dehydrated use sodium chloride 0.9% as rehydration fluids
Hypernatraemic dehydration (Na>160mmol/L)
 Give sodium chloride 0.9% (or compound sodium lactate (Hartmann’s solution)) and
correct deficit slowly (over 48 hours) to reduce the risk of neurological injury associated
with a rapid fall in plasma sodium. The correction rate should be by no more than
12mmol/24hr. Sodium chloride 0.45% can also be used.
HONK.
This usually occurs in elderly patients with NIDDM and can develop over days or weeks;
glucose levels are often >30mmol/l.
It often occurs with intercurrent illness, especially infection.
Patients are usually severely dehydrated and there is impairment of consciousness.
Diagnosis is made by:
i)
ii)
ii)
hyperglycaemia with osmolality >350mmol/l (normal 280-305)
no acidosis
<++ ketones on urinalysis
There may be a coexistent lactic acidosis (which implies a poor prognosis).
Suggest 4 essential investigations.
ABG, blood glucose, septic screen, ECG ~ look for evidence of infection and AMI or myocardial
ischaemia.
Apart from ABC, what should the initial treatment be?
Mainstays of treatment are fluid resuscitation and insulin.
 IV fluids:
1l in 1hr
1l in 2hrs
1l in 2 hrs
then continue with 1l every 4hrs.
 if Na+ <160mmol/l use normal saline
if Na+ >160mmol/l use ½ normal saline
 K+ is usually normal; no K+ in first litre of fluid, subsequent replacement depends on K+ level.
 Insulin infusion commenced (50U Actrapid in 50ml N/saline – start at 3U/hr) to maintain fall of
about 3-6mmol/hr.
 Full anticoagulation with heparin.
 May need catheter and CVP line.
 NG tube if consciousness impaired.
 Treat underlying cause if found e.g. UTI.
 ICU/ HDU admission.
Current guidelines for tetanus prophylaxis
Standard active immunisation involves an initial course of 3 doses of tetanus toxoid at 2, 3 and 4 months
of age followed by booster doses at 4yrs and 14yrs.
A full course of 5 doses is considered to give lifelong immunity.
Inadequate immunity against tetanus is likely in immigrants, the elderly, patients who are immunesuppressed and those who have refused vaccination.
The following wounds are regarded as ‘tetanus prone’:
i)
ii)
iii)
iv)
heavy contamination (esp. soil or faeces)
devitalised tissue
infected or wounds >6hrs old
puncture wounds and animal bites
For fully immunised patients, a dose of human anti-tetanus immunoglobulin (HATI, 250U IM) is only
necessary for very high-risk wounds. For other patients, continue/ begin the standard schedule and give
HATI for tetanus-prone wounds.
Standard immunisation schedule:
2 months
3 months
4 months
12-15 months
3-5yrs
10-14yrs
13-18yrs
D, T, P, polio, Hib, meningitis C
D, T, P, polio, Hib, meningitis C
D, T, P, polio, Hib, meningitis C
MMR
D, T, P, polio, MMR
BCG
D, T, polio
WPW question.
Impulses are conducted from the atria via the AV node and an accessory pathway (bundle of Kent). The
accessory pathway conducts more quickly than the AV node so the PR interval is short. The region of
ventricle activated by the accessory pathway slowly depolarises giving rise to a delta wave. Shortly
afterwards the rest of the ventricular muscle is depolarised by the arrival of the impulse from the AV
node.
It is one of the commonest causes of tachyarrhythmias in children (may be accompanied by palpitations,
dizziness, faints, chest pain) but can be asymptomatic. In infancy 80% are idiopathic but other causes
include ASD and cardiomyopathy.
It can present with AF associated with WPW ~ consult cardiology as this a potentially dangerous
rhythm.
Patients with WPW should not be given drugs that block the AV node (digoxin, calcium channel blockers)
as this can result in acceleration of conduction through the accessory pathway leading to VF.
Cure may be achieved by radiofrequency ablation.
Adenosine acts by slowing conduction through the AV node. Maximum dose is 12mg. It has a very short
half-life. CI include 2nd or 3rd degree heart block, sick sinus syndrome, AF and atrial flutter. Caution in
patients with asthma as it may induce bronchoconstriction.
Burn:
What are the fluid requirements?
4ml X (burn surface area) X (body weight (kg))
50% given in first 8 hours, 50% over next 16 hours. Object is to obtain urine output of 1ml/kg/hr.
Children receive maintenance requirements in addition to above amount.
Q)
A 3 year old child presents after 4 days of D&V. He is afebrile with a
rate of 150.
What is his maintenance fluid requirement?
Need to calculate percentage dehydration:
Mild (<5%)
Thirst
Dry mouth
Concentrated urine
Moderate (5-10%)
Sunken fontanelle/ sunken eyes
↓urinary output (<4 wet nappies/24hrs in a baby)
Tachypnoea
Tachycardia
dry mouth and a pulse
Severe (>10%)
Hypotension (very late)
Skin turgor
Drowsiness/ irritability
Maintenance requirements are:
100ml/kg/day for first 10kg
50ml/kg/day for next 10kg
20ml/kg/day for each subsequent kg
So his maintenance requirements are:
Estimated weight (age+4) X 2 = 14kg
(10 X 100) + (4 X 50) = 1200ml
Assume deficit of 10%:
10 X 10(%) X 14 = 1400ml
So total daily requirement is 2,600ml. Use 0.45% saline/ 5% dextrose if not able to tolerate oral
rehydration or is deteriorating.
APGAR scores:
APGAR scores are done at 1 and 5 minutes post delivery.
2
1
0
Heart rate
>100
<100
Absent
Respirations
Good, crying
Slow, irregular
Absent
Muscle tone
Active motion
Some flexion
Limp
Reflex irritability
(catheter in nares)
Cough or sneeze
grimace
No response
Colour
Completely pink
Pink body, blue limbs
Blue or pale
Remember if you need to cannulate the umbilical vein (fastest method of venous access in newborn) it
is the single large dilated vessel adjacent to the 2 constricted arteries. Insert a 5F catheter 5cm into the
vein and secure with a tie.
.
chickenpox pneumonia in a child ~ remember this is usually staphylococcal in children.
Dendritic Ulcer of cornea:
Give 3 features of management.
i)
Analgesia
ii)
Topical acyclovir 3% X5/d
iii)
Refer ophthalmology
Pre-eclampsia:
List 6 symptoms/signs of pre-eclampsia.
i)
Headache
ii)
Visual disturbance
iii)
Hyperreflexia
iv)
Abdominal pain
v)
Tremor
vi)
Reduced urine output
List 4 risk factors for pre-eclampsia.
i)
Primiparity.
ii)
Maternal systemic disease – DM, renal disease, hypertension.
iii)
Low socioeconomic status.
iv)
Maternal age <20 or >35 years.
Give 3 immediate treatments.
i)
beta-blocker / Hydralazine 5mg IV over 20mins to max. 20mg.
ii)
Careful fluid balance; preload of 500ml colloid prior to hydralazine may reduce risk of
hypotension and fetal distress.
ii)
Magnesium sulphate 4g IV over 5-10 minutes followed by maintenance of 1g/hr for 24hrs.
What are the signs of magnesium toxicity?
Loss of deep tendon reflexes and respiratory depression.
What strategies can be used to facilitate suturing of the wound with minimal distress to the child?
i)
Distraction/ play techniques.
ii)
Suitable environment.
iii)
Reassurance by good interaction with carers/ parents.
iv)
Oral analgesia.
Ramsay-Hunt syndrome.
Facial nerve palsy caused by herpes zoster infection of the geniculate ganglion.
There may also be loss of taste on the anterior part of the tongue, tinnitus, hearing loss and vertigo.
Give analgesia and refer to ENT for IV acyclovir and eye care.
Sickle cell crisis:
Outline your initial treatment.
i)
Keep patient warm, rested and give O2.
ii)
Opioid analgesia is usually required for pain.
ii)
Careful rehydration with fluids – crystalloid.
iv)
Empirical antibiotic therapy e.g. cefuroxime 750mg IV tds.
v)
Exchange transfusion may be required; aim for Hb between 7-9g/dl as
blood viscosity and precipitate further sickling.
any higher can increase
List the most useful investigations
i)
FBC
ii)
Infection screen – blood culture, CXR, MSU
iii)
U&E, ABG, ECG
Patients with sickle cell trait usually have no disability except at times of severe hypoxia. Patients with
sickle cell anaemia have chronic anaemia (8-10g/dl) and a small percentage have recurrent crises.
Later in life, chronic ill-health supervenes with renal failure, bone necrosis, osteomyelitis (Salmonella),
there is an increased susceptibility to infection, leg ulcers.
Sickle cell crises can occur spontaneously or follow infection, cold, dehydration or any situation where
tissue hypoxia exists. Acute medical and surgical emergencies may be mimicked.
i)
Acute painful crises are the most common presentation; severe pain at one or more sites
associated with pyrexia, tenderness and local warmth and swelling. Haemolysis may be increased –
there is a fall in Hb and reticulocyte count is increased. There are no reliable markers to
indicate
severity.
ii)
Chest crisis is the most common cause of mortality. There is vasoocclusion
of
pulmonary microvasculature resulting in local infarction. May be precipitated by infection.
iii)
Cerebral infarction: usually children <5yrs, rare in adults. Presents as
the
acute stroke.
iv)
Splenic/ hepatic sequestration: usually children <5yrs, RBCs become
liver, causes severe anaemia and circulatory
collapse.
trapped in spleen and
v)
Aplastic crisis: usually in children and young adults, mainly caused by
Reduced reticulocyte count.
parvovirus infection.
vi)
Urological emergency.
Priapism: Local vaso-occlusion causes prolonged, painful erections.
Q.
25 year old man admits to regular use of
crack cocaine. He has presented with SOB and
pleuritic chest pain.
Clinical examination is unremarkable.
What is the diagnosis?
Crack pneumonitis.
Give 3 differential diagnoses.
i)
Atypical pneumonia.
ii)
Sarcoidosis.
iii)
Extrinsic allergic alveolitis.
Respiratory complications of crack use can include pneumonitis, infections, pulmonary oedema,
pulmonary fibrosis and ARDS.
Q.
A 5 month old boy presents with fever, irritability and vomiting. His temperature at
home was 38.0. He has vomited 5 times since yesterday. Past medical history is
unremarkable.
On examination he does not focus or interact well. Anterior fontanelle is full but he is crying. PEARL.
Normal muscle tone. No other abnormalities.
What is the differential diagnosis?
i)
ii)
iii)
iv)
Meningitis.
Septicaemia.
Encephalitis.
Shaken baby syndrome.
Cerebello-pontine angle lesions:
Acoustic neuroma.
other lesions that occur in this area.
i)
ii)
iii)
iv)
v)
cholesteatoma
meningioma
neuromas of CN V, VII, X
basilar artery aneurysm
medulloblastoma
What cranial nerves may be affected by such lesions?
V-XI
Vth nerve symptoms most common; depression of the corneal reflex occurs early. Facial pain,
paraesthesiae and numbness may develop.
Large tumours may compress cerebellum, pons and 4th ventricle.
Retinopathy and malignant hypertension.
Early signs of retinopathy correlate less well with mortality and morbidity than used to be thought, but
signs of accelerated or "malignant" hypertension indicate severe illness.
Symptoms
Most patients with hypertensive retinopathy present without visual symptoms, however, some may
report decreased vision or headaches.
Signs of damage to the retina caused by hypertension include:






Arteriosclerotic changes
o Arteriolar narrowing that is almost always bilateral
 Grade I - 3/4 normal caliber
 Grade II - 1/2 normal caliber
 Grade III - 1/3 normal caliber
 Grade IV - thread-like or invisible
o Arterio-venous crossing changes (aka "AV nicking") with venous constriction and
banking
o Arteriolar color changes
 Copper wire arterioles are those arterioles in which the central light reflex
occupies most of the width.
 Silver wire arterioles are those in which the central light reflex occupies all of the
width of the arteriole.
o Vessel sclerosis
Ischemic changes (e.g. "cotton wool spots")
Hemorrhages, often flame shaped.
Edema
o Ring of exudates around the retina called a "macular star"
Papilledema, or optic disc edema, in patients with malignant hypertension
Visual acuity loss, typically due to macular involvement
Exams and Tests



Blood pressure
Fluorescein angiography
Ophthalmoscopic examination, which can show changes even if you have no symptoms
Retinal changes mirror the systemic circulation and their severity correlates well with the development
of systemic complications and survival
 Grade 1 consists of “mild” generalized retinal arteriolar narrowing;
 grade 2 consists of “more severe” generalized narrowing, focal areas of arteriolar narrowing,
and AV nicking;
 grade 3 consists of grade 1 and 2 signs plus the presence of retinal hemorrhages,
microaneurysms, hard exudates and cotton wool spots; and
 grade 4, sometimes referred to as accelerated (malignant) hypertensive retinopathy, consists of
signs from the three previous grades with the addition of optic disc swelling and macular
edema.

One of the major limitations of this classification system is the difficulty in distinguishing early
hypertensive retinopathy grades (e.g., grade 1 from grade 2);
. Patients with mild hypertensive retinopathy signs will likely require routine care and blood pressure
control should be based on established guidelines. Patients with moderate hypertensive retinopathy
signs may benefit from further assessment of cardiovascular risk (e.g., cholesterol levels) and, if clinically
indicated, appropriate risk-reduction therapy (e.g., cholesterol-lowering agents). Patients with severe
hypertensive retinopathy will continue to need urgent, immediate, anti-hypertensive management
Diabetic retinopathy is the most frequent cause of new cases of blindness amongst adults aged 20-74
years. Diabetic retinopathy is classified as:
Background
Maculopathy
Pre-proliferative
Proliferative
dot and blot haemorrhages, microaneurysms, exudates
macular oedema
↑ cotton wool spots, dot and blot haemorrhages
new vessel formation
Remember there may be evidence of laser therapy.

Grade 1 (US) Haemorrhages & microaneurysms only Mild non-proliferative (mild preproliferative)
 Grade 2 (US)
Extensive Microaneurysm, intraretinal haemorrhage, and hard exudates.
Moderate non-proliferative, moderate pre-proliferative
 Grade 3 (US)
Previously termed severe pre-proliferative. Venous abnormalities, large blot haemorrhages, cotton wool
spots (small infarcts), venous beading, venous loop, venous reduplication,
 Grade 4a (US)
Proliferative retinopathy. New vessel formation either at the disc (NVD) or elsewhere (NVE). Cl/fFloaters, sudden visual loss
 Grade 4b (US).
Extensive fibrovascular proliferation, retinal detachment, pre-retinal or vitreous haemorrhage,
glaucoma, Traction . Subhyaloid haemorrhage
Pre-retinal fibrosis+/- tractional retinal detachment
National Screening Committee
The National Screening Committee (NSC) propose the following classification. Some centres use a more
detailed classification, based onthe NSC system proposal. The condition is graded by examination of
digital retinal photographs.
Abreviations:

DR = diabetic retinopathy

NPDR = non-proliferative retinopathy

NVE = new vessels elsewhere

IRMAs = intraretinal microvascular abnormalities (part of severe pre-proliferative retinopathy,
vessels will not leak with angiogram, otherwise they would be 'new vessels' making the
condition 'proliferative')
NSC
International
Term
Symptoms
Features (see)
Action
R0
No DR
None
Normal retina. Grade 0 (US)
annual rescreen
RI
Mild nonproliferative (mild
pre-proliferative)
None
Haemorrhages & microaneurysms only only
see photo
Grade 1 (US)
Inform diabetes
team
R2
Moderate nonproliferative,
moderate preproliferative
None
Previously termed mild pre-proliferative.
Extensive Microaneurysm, intraretinal
haemorrhage, and hard exudates. See
photo and photo Grade 2 (US)
refer HES
R2
Severe nonproliferative
None
Previously termed severe pre-proliferative. urgent refer
Venous abnormalities, large blot
HES
haemorrhages, cotton wool spots (small
infarcts), venous beading, venous loop,
venous reduplication, IRMA, See photo and
photo .
Grade 3 (US)
Proliferative
retinopathy
Floaters,
sudden
visual loss
New vessel formation either at the disc
(NVD) or elsewhere (NVE).
Photos: flat new vessels, raised, florid
Grade 4a (US)
urgent refer
Pre-retinal
fibrosis+/tractional retinal
detachment
Floaters,
central
loss of
vision
Extensive fibrovascular proliferation, retinal
detachment, pre-retinal or vitreous
haemorrhage, glaucoma. Grade 4b (US).
Traction photo and photo. Subhyaloid
haemorrhage photo
urgent refer
HES
no maculopathy
annual rescreen
The macula is defined as a circle centred on
the fovea, with a radius of the distance to
the disc margin. If the leakage involves or
is near the fovea the condition is termed
clinically significant macular oedema
(CSME).
Exudative maculopathy presents with
leakage , retinal thickening,
microaneurysms, hard exudates at the
macula. Ischaemic form can have a
featureless macular with NVE and poor
vision.
refer HES
severe preproliferative
R3
R3
M0
M1
Diabetic
maculopathy
Blurred
central
vision
HES
Photos: moderate, severe
Milder forms:

exudate < or = 1DD of centre of
fovea

circinate or group of exudates
within macula

any microaneurysm or
haemorrhage < or = 1DD of centre
of fovea only is associated with a
best VA of < or = 6/12
retinal thickening < or = 1DD of
centre of fovea (if stereos available)
P
Photocoagulation
OL/
UG
Other lesion / Ungradable
Reduced
night
vision,
glare
Small retinal scars through out the
peripheral retina. Grade 4b (US)
Un-gradable is usually due to cataract,
other lesions usually referred for
assessment
Clinical Examination
Examination can also be carried out using an ophthalmoscope. This should include use of the green filter
(red free) as It shows haemorrhages and new vessels much more easily, see . The slit lamp is very useful
clinically.
Q.
This patient has recently started lamotrigine.
What is this rash?
Toxic epidermal necrolysis. This is an immunological disease most often caused by adverse drug
reactions (antibiotics, NSAIDs, anticonvulsants).
Non-drug causes include viral and bacterial infections, idiopathic and malignancy.
Thought to be related to Stevens-Johnson syndrome.
Needs to be distinguished from staphyloccocal scalded skin syndrome (skin biopsy).
It is a potentially life-threatening emergency as
the patient may develop dehydration, eye problems, renal involvement leading to ARF, systemic
infections, shock and MOF.
Management consists of treating cause, supportive care, prevent complication
angioneurotic oedema (C1-esterase inhibitor deficiency).
Autosomal dominant inheritance, usually presents in 2nd decade.
May also be acquired as paraneoplastic syndrome.
Clinical features;
i)
S/C oedema affecting face, limbs, buttocks, genitals (91%).
ii)
laryngeal oedema (48% of attacks).
iii)
abdominal symptoms.
Precipitating factors include stress, infection, OCP, ACE inhibitors
Management of severe attacks may require;
i)
chlorpheniramine 10mg IV
ii)
hydrocortisone 200mg IV
iii)
adrenaline 0.5ml of 1:1000 S/C
iv)
FFP or C1-esterase inhibitor plasma concentrate
Diagnosis made by low complement C4 levels.
A-a gradient (Alveolar-arterial oxygen gradient).
In the EM setting the A-a gradient is usually used to evaluate patients with a suspected pulmonary
embolus. It is a fairly reliable measure of oxygen exchange.
Unfortunately there appear to be lots of different formulae, using different units, calculating at sea level
etc……
My formula, using kPa as units is:
FiO2-(PaO2+(PaCO2/0.8))
Where 0.8 is the respiratory quotient.
A normal A-a gradient is less than 2kPa when breathing air; it may reach 4kPa in the elderly. An
increased A-a gradient identifies decreased oxygen in the arterial blood compared to the oxygen in the
alveolus. This suggests a process that interferes with gas transfer, or in general terms, suggests
ventilation-perfusion mismatch. A normal A-a gradient in the face of hypoxemia suggests the hypoxemia
is due to hypoventilation and not due to underlying lung disorders.
However neither measured PaO2 (18% normal) nor the A-a gradient (6% normal) are reliably sensitive in
predicting PE.
What in a chronic alcoholic predisposes them to fitting? (4 marks)
Hypoglycaemia/Excess Alcohol or Alcohol Withdrawal
Hyponatraemia
Falls & ICH
Poor compliance to anticonvulsants
Hepatic Encephalopathy
Overdose of TCAs
Community acquired pneumonia in children
PCR and other investigations suggest commonest organisms are- viruses, mycoplasma, pneumococci
and pertusis.
Types
 Lobar pneumonia- toxic and ill child with fever, classical signs of consolidation. Usually due to
pneumococci, and associated with effusion.
 Atypical or patchy pneumonia– more common than lobar pneumonia, usually caused by
mycoplasma, also chlamydial, viral or legionella.
Oral treatment- clarithromycin or amoxicillin
i.v. treatment- Penicillin 25 mg/kg qds (or cefuroxime 20 mg/kg tds in resistant case) and oral
clarithomycin 7.5 mg/kg bd
If child remain unwell and pyrexial after 48 hrs- treatment failure – due to
 antibiotics resistant
 underlying condition such as empyema, cystic fibrosis, ciliary dyskinesia, broncheictasis, tracheaoesphageal fistula,
 immune-deficiency
 poor compliance
Pertusis can cause severe illness and even death during the first year of life.
X-ray showing abscess may be secondary to staph aureus, klebsiella or TB.
Hospital acquired pneumonias have different organisms, contact microbiologists.
Children with special need (eg paraplegia, scoliosis, muscular dystrophy) have different
pathophysiology- aspiration, reflux and poor lung function. Management is very difficult. Chest
physiotherapy, suctioning and good general care is very important.
Immunocompromised children (neutropenia, on chemotherapy, risk of HIV) – risk of PCP, patient may
have respiratory distress with few or no chest signs, chest x-rays may be non-specific . a firm diagnosis
require broncho-alveolar lavage or sputum induction after saline nebulizer. Microbiologist should be
contacted. Treatment- co-trimoxazole 120 mg/kg in two divided doses.
Recurrent chest infection- think of asthma
Palivizumab is a monoclonal antibody developed for the prevention of serious lower
respiratory tract infections caused by RSV.
Palivizumab immunisation will be offered to:
1. All infants under 2 years of age with chronic lung disease of prematurity who are
on home oxygen at the start of the RSV season (RSV season is from beginning of
October until March).
2. All preterm infants on the NICU with chronic lung disease (requiring continuous
supplementary oxygen at 36 weeks corrected gestational age and likely to be
discharged on supplementary home O2 during the RSV season.
3. Children under 2 years of age with severe congenital immuno-deficiency
e.g. Severe combined immunodeficiency, or Di George syndrome with T-cell
abnormality.
4. Infants with severe (haemodynamically significant) congenital cardiac disease who
are aged 12 months or younger at the start of the RSV season.
5. Palivizumab immunisation may be considered on an individual basis for rare
conditions such:
 Severe multiple congenital abnormalities
 Tracheomalacia
 Recurrent aspiration
 Neuromuscular disorders
Diarrhoea:
The following features may be indicative of diagnoses other than acute viral gastroenteritis;
 Abdominal pain with tenderness/guarding and/or bilious vomiting (?surgical)
 Pallor, jaundice, oligoanuria, bloody stool (?HUS)
 Systemically unwell, out of proportion to the level of dehydration (other infections, surgical,
CAH etc)
 Shock
Category
Examples
Infections
Enteral: viral (commonest cause), bacterial, parasitic
Non enteral infections (UTI, pneumonia, Otitis media)- vomiting
predominates
Surgical
Appendicitis, Intussusception, Obstruction, Short bowel syndrome
Systemic illness
Endocrinopathy (Diabetes, Hyperthyroidism, Congenital Adrenal
Hyperplasia, Addison’s disease, hypoparathyroidism),
Immunodeficiency.
Antibiotic
associated
Miscellaneous
Whilst taking antibiotics and rarely Pseudo-membranous colitis
Dietary
disturbance
Food allergy/ intolerance (Lactose, Cows milk protein), starvation
stools.
Malabsorption
Cystic fibrosis, Coeliac disease,
Inflammation
Ulcerative colitis/ Crohn’s, Hirschsprung’s enterocolitis
Idiopathic/
Psychogenic
Irritable bowel syndrome
Constipation with overflow, Toxins, Haemolytic-uraemic syndrome
(HUS), Toddler diarrhoea, Child Abuse (Munchausen by proxy,
sexual)
Calculation of Oral Rehydration Solution (ORS) requirements in dehydration.


Mild to Moderate (3% - 8%)
dehydration.
Severe dehydration (>9%)
30 to 80mls per Kg in 4 hours
100mls per Kg in 4 hours
Practical Points:
*Children who are dehydrated are thirsty and do not normally refuse ORS.
*Give fluid little and often. If the child is vomiting decrease volumes and increase frequency (every 5-10
minutes).
*Where carers are not willing/able to do this under supervision (or child is asleep) then rehydrate by
NGT.
*Suitable ORS are Dioralyte, Diocalm Junior or Electrolade.
Ongoing losses:
These requirements should be supplemented if the child has frequent or substantial watery stools or
vomits, by an additional 10ml/Kg per stool/vomit.
Table 5: When to send a stool to the lab for microscopy, culture, sensitivity and virology.

A history of blood +/- mucous in the stool

Systemically unwell, severe or prolonged diarrhoea

If the child is admitted to hospital

A history suggestive of food poisoning (Notify public health)

Recent travel abroad
Management of feeding during gastroenteritis.

Breast fed
Continue breastfeeding throughout rehydration and maintenance phases

Formula fed
Restart feed at full strength as soon as rehydration complete (ideally 4 hours)

Weaned
children
Child’s normal fluids and solids following rehydration. Avoid fatty foods or
foods high in simple sugars.
Guide to drug treatment.
 Antidiarrhoeals Infants and Children should not be treated with antidiarrhoeal agents.

Antibiotics
Patients with invasive Salmonella typhi, Shigella, amoebiasis and Giardiasis
should be treated with antibiotics.
Consider in infants<6months with other salmonellas, those who are
systemically unwell and the immunocompromised.
(Notify public health where necessary)
Clostridium difficile associated diarrhoea


Clostridium difficile diarrhoea is a common side effect of antibiotic use.
Key steps in the prevention and management of C.difficile include:
o
Prudent use of antibiotics
 Narrow spectrum preferably
 Short courses recommended
 Wherever possible, avoid use of high risk  lactams (amoxicillin, co-amoxy-clav),
clindamycin, cefalosporins and/or quinolones.
o
Isolation of confirmed/suspected cases
 Ensure affected patients are nursed in single rooms, with Enteric precautions (see
page 25)
 When dealing with clusters of cases, follow the guidance of the Infection
Prevention & Control Team re: cohort nursing.
 Ensure Bristol stool chart is used to guide management.
 Patients should be isolated on suspicion of Clostridium difficile associated
diarrhoea (CDAD), and not more than 2 hours after a result is confirmed.
o
Hand Hygiene
 In all infective gastrointestinal cases, hand hygiene with hot soapy water is
recommended.
o
Specific treatment recommendations
 See section 3.2 p.9
 Review cases daily, and escalate treatment if patient not responding as per above.
The diarrhoea and colitis occur as consequences of toxins secreted by C.difficile.
The clinical picture in C.difficile infection may vary from mild diarrhoea through to the fulminant lifethreatening pseudomembranous colitis.
Diagnosis of Clostridium difficile diarrhoea
Microbiological Examination of C.difficile Toxin (CDT)
The toxin biodegrades at room temperature (increasing the possibility of false negatives results),
stool samples should therefore be placed in a refrigerator if there is to be any delay in
transportation. If the first stool sample is negative for CDT, another sample should be sent for
examination before the patient is considered to be CDT negative.
Sigmoidoscopy (excludes haematology and neutropenic patients)
Flexible sigmoidoscopy may detect pseudomembranous colitis in patients with a negative
Clostridium difficile toxin test, and may need to be considered, in patients with moderate/severe
diarrhoea (>4 x day) not responding to supportive measures and one stool sample negative for
Clostridium difficile cytotoxin
Management of Clostridium difficile associated diarrhoea
General Measures






Discontinue precipitating antibiotics if possible
If not possible to stop antibiotics, alter the regimen to use antibiotics with a lower risk of
exacerbating Clostridium difficile associated diarrhoea
Discontinue antiperistaltic agents (opioids, anti-diarrhoeal agents etc.)
Discontinue promotility/prokinetic agents (laxatives, stool bulking agents etc.)
Review use of proton pump inhibitors and discontinue if possible
No additional treatment is necessary if the stools have become formed or semi-formed and the
patient is well.
Antimicrobial Treatment
Treatment of mild to moderately severe Clostridium difficile diarrhoea and colitis
First line:
Second line:
Metronidazole 400mg tds po (500mg tds IV) for 10 days
Vancomycin 125mg qds po for 10 days
Vancomycin therapy should be used in patients:
 Who have failed to respond to 3-5days of oral metronidazole therapy
 Critically ill patients
 Severe pseudomembranous colitis
 Unable to tolerate metronidazole
 Pregnant
 Where the infecting organism proved to be metronidazole resistant
Treatment of severe disease and/or pseudomembranous colitis
Severe Clostridium difficile diarrhoea and colitis

Critically ill
o
WBC > 15 x 109 cells/L
o
Temperature > 38.3ºC
o
Albumin < 25g/L

Impending ileus

Colonic dilation

Fulminant pseudomembranous colitis (endoscopic evidence)
First line: Vancomycin 250-500mg qds po for 10 to 14 days
Additional information

Oral antibiotics are preferred as they act directly on the gut, (IV Vancomycin has no
useful penetration into the gut).

If a patient cannot swallow, the PR route (for metronidazole) or syrup via a PEG are
equally effective.

Clinical progress must be reviewed daily. If condition worsens, or there is no
evidence of diarrhoea settling after 3 days, change from Metronidazole/low dose
Vancomycin treatment to Vancomycin 250mg po qds for 10-14 days*.

Consult duty Medical Microbiologist if any of the above and/or persistent failure to
respond.
Treatment of recurrences
Initial recurrence:
Treat with the same antibiotic that was effective for the treatment
of the first Clostridium difficile positive stool, either Metronidazole
400mg tds po or Vancomycin 125mg qds po for 10 days (250500mg qds po for 10 to 14 days for severe colitis)
There may be a role for IV immunoglobulin (400 mg/kg, as a single infusion), under the guidance and
advice of a Consultant Gastroenterologist.
Surgical Treatment
Patients with clinical features indicative of likely 027 type infection and/or evidence of
pseudomembranous colitis will need urgent surgical referral. Colectomy must be considered, as it may
be life saving, and advantages vs. disadvantages assessed based on a surgical opinion.
Infection Control Aspects
Prevention of spread

Isolation/Cohort nursing:
These spores are resistant to alcohol and acids in the stomach. They can also survive in patients and the
surrounding environments for long periods of time.
Isolate symptomatic patients at the onset of symptoms in a single room, preferably with en-suite toilet
facilities. An Enteric Isolation poster should be clearly displayed,
If a single room is not available, or if there are several infected patients, then it may be more
appropriate to cohort affected patients together. Affected patients should be nursed in a bay area with
doors, away from immunocompromised patients and not on the main route for ward and near to hand
hygiene facilities. Duration of isolation.
Isolation may be discontinued when the patient has been symptom free (formed stools) for at least 72
hrs as the main infection source is faeces. There is no requirement to submit further faeces samples for
toxin detection, as toxin may be present in the gut for a time after the patient has become
asymptomatic. When patients have been symptom free for 72 hours, they should be moved to a clean
bed in a clean environment (single room or bedspace), taking with them only their personal belongings.


Hand Hygiene: Visitors + Staff + patients’ hands
Movement of patients:
Discharges and ward transfers. Patients with explosive C.
difficile diarrhoea should not be transferred to other wards in the hospital, except for purposes
of isolation or cohort nursing. Visits to other departments should be kept to a minimum. These
patients should be seen at the end of the session and should only be sent for when the
department is ready to see them; they should not be left in a waiting area with other patients.

Stool Chart

Information leaflet
Staff should wear disposable aprons, gloves and visors when dealing with faecal material. Meticulous
infection control procedures should be employed when dealing with faecal material.
 All discharge summaries MUST clarify if the patient is now or has during this recent admission
suffered from diarrhoea.
 Room cleaning (clinical clean) Following discharge/ transfer of the patient, the room and its
contents should be cleaned thoroughly.
Outbreaks of C.difficile

5.1
Clostridium difficile outbreaks are expensive, disruptive to the delivery of healthcare services
and often result in prolonged in-patient care. Wards and services are likely to be closed
temporarily with consequent difficulties admitting urgent and waiting list patients. Prompt and
vigorous control measures taken as soon as a problem of Clostridium difficile infection is
recognised are the best way of ensuring the safety of patients and continued hospital activity.
Definition of an Outbreak
C difficile figures for the Trust are reviewed daily and weekly by the Infection Control Team.
A risk assessment is carried out when the number of C difficile cases on a ward exceeds the
average base line, or when the cases of C. difficile are not obviously related to antimicrobial
therapy.
The Infection Control Team will normally consider:



What is normal background level of Clostridium difficile in the clinical area?
Is the diarrhoea attributable to any other cause i.e. medication or surgery?
Is there any time/special relationship between the cases?
If an outbreak situation is considered likely, the Infection Prevention and Control Team will advise
further action and implement necessary Infection Control measures.
A decision will be made by the Director of Infection Prevention & Control and the Team will contact the
Health Protection Unit and the Primary Care Trust (Commissioning) regarding any closures.
A Serious Untoward Incident (SUI) report will be sent to the Strategic Health Authority. This will be
completed by the Saving Lives Lead, under the direction of the Risk Manager with support from the
Infection Prevention and Control Team.
Management of an Outbreak
Patients should be cohort nursed and staff allocated for their care. Enteric precautions should be
employed, as previously described. The ward may be closed to admissions and transfers.
Clearance and Repeat specimens
a)
Symptoms resolve – no further C difficile toxin test required.
b)
Symptoms persist despite treatment – further Clostridium difficile testing only justified at
least 4 weeks after the previous test.
c)
Symptoms resolve then recur – repeat Clostridium difficile testing is justified to diagnose
relapse of the condition. There is a risk of relapse of symptoms in 20 – 30% of patients.
d)
Initial negative test, but symptoms persist – only in exceptional circumstances and with
particular clinical suspicion (i.e. diagnosis of pseudomembranous colitis). Liaison with
the Consultant Microbiologist is recommended by senior clinician.
Ciprofloxacin and cephalosporins are currently considered to be high risk of precipitating Clostridium
difficile infection
Prescribing in Penicillin allergy:
 Patients with a history of anaphylaxis or urticaria occurring immediately after penicillin therapy
are at increased
risk of immediate hypersensitivity to penicillins and should not receive treatment with a betalactam antibiotic
(this includes cephalosporins) or carbapenem, unless they have previously received a betalactam and had no
adverse effects
 Patients with a history of rash occurring more than 72 hours after administration of penicillins
are probably not
allergic to penicillins, (SIGN, 2000) and many patients with a history of rash after penicillins will
have received
cephalosporins with no ill effect. For patients who do NOT report an anaphylactic or urticarial
response to
penicillin a cephalosporin or carbapenem (e.g. meropenem) may be administered with caution.
 Please note that penicillins include amoxicillin, co-amoxiclav (Augmentin®), flucloxacillin,
Tazocin®.
Patients who are prescribed ciprofloxacin, clindamycin or a cephalosporin should be counselled what to
do if diarrhoea develops.
Biliary tract infection(including cholangitis and cholecystitis) and Abdominal infection e.g. perforation,
peritonitis ,diverticulitis (excludingCAPD peritonitis) (including if due to appendicitis)
If gentamicin contraindicated and a cephalosporin tolerated
Cefuroxime 1.5g tds IV + Metronidazole 500mg tds IV
In truly penicillin allergic patients use
Metronidazole 500mg tds IV + Gentamicin# 5mg/kg
IV (single daily dose regimen) Max 480mg



Amoxicillin 1g tds IV and
Metronidazole 500mg tds IV and
Gentamicin 5mg/kg IV (single daily dose regimen) Max 480mg
If Gentamicin contraindicated use Co-amoxiclav 1.2g tds IV (or in serious sepsis Tazocin® 4.5g tds IV) in
place of above regimen. Review after 48 hours.
Suitable oral regimens include co-amoxiclav 625 mg po tds OR Ciprofloxacin 500mg bd po (in truly
penicillin allergic patients) plus Metronidazole po 400mg tds.
Co-amoxiclav has good anaerobic activity, therefore the addition of metronidazole is not usually
indicated.
Meningitis – Treatment
 If meningococcal disease suspected: Benzylpenicillin 1.8g 2-hourly IV or 2.4g 4-hourly IV for 1224 hours followed by 2.4g 4-hourly IV for 7 to 10 days
 If causative organism unknown: Cefotaxime 2g tds IV for 7 days
 If causative organism unknown and/or Cephalosporins (penicillin allergy) are also
contraindicated: Chloramphenicol 500mg qds IV (consult microbiology for advice)
Meningitis – Prophylaxis for H.influenza and N.meningitis (not normally required for Strep pneumoniae)
 Rifampicin 600mg bd po for 2 days or
 Ciprofloxacin 500mg po single dose (unlicensed indication)
Meningitis associated with operative interventions or intracranial device will require consideration of
other pathogens. Discuss with Consultant Medical Microbiologist.
Severe cellulitis (gastrointestinal/biliary tract NOT entered, i.e non-surgical)
 Benzylpenicillin 1.2-2.4g qds IV and Flucloxacillin 1-2g qds IV for 5-10 days depending on
progress, OR
 Once daily Ceftriaxone 2g IM if treated as outpatient
In penicillin allergy:
 Clarithromycin 500mg bd IV for 5-10 days depending on progress, OR
 Teicoplanin IM if treated as outpatient
Severe cellulitis (gastrointestinal / biliary tract entered i.e. post surgery) or necrotising fasciitis
 Tazocin® 4.5g tds IV. Review after 48 hours and step down to oral therapy: Co-amoxiclav 625 mg
tds po
In Penicillin allergy,

If carbapenems tolerated and if gentamicin contra-indicated (see below) use Meropenem
500mg-1g tds IV
In truly penicillin allergic patients use
 Gentamicin 5mg/kg IV (single daily dose regimen) and
 Clarithromycin 500mg bd IV and
 Metronidazole 500mg tds IV
Review after 48 hours and step down to oral therapy:
 Clarithromycin 500mg bd po and
 Metronidazole 400mg tds po
Respiratory tract infection by MRSA
Doxycycline (PO 200mg stat then 100mg od 1/52)
OR 2nd LINE
Clindamycin following medical microbiologist approval only (PO 300mg qds 1/52)
+
Rifampicin (PO 300mg qds 1/52)
Osteomyelitis (Therapy 4-6 weeks) / Septic arthritis (Therapy usually 2-4 weeks)
Staph aureus identified or, no other suggested sources
 Flucloxacillin 1 – 2 g qds IV and Sodium fusidate 500mg tds po, or
 Vancomycin* 1g bd IV and Sodium fusidate 500mg tds po, OR
 Vancomycin* 1g bd IV and Rifampicin 600mg bd po
Neutropenia/Immunocompromised patients- Prophylaxis
Prophylaxis for patients in whom prolonged (>7 days) neutropenia anticipated (e.g. acute leukaemia
treatment)
 Ciprofloxacin 250mg bd po, and
 Fluconazole 100mg stat po and 50mg od po Monday, Wednesday and Friday
 If strong history of significant/recurrent cold sores or mouth ulcers add in: Aciclovir 200mg tds
po
Prophylaxis in patients received chemotherapy where only a short period of neutropenia is expected.
Antimicrobial prophylaxis is NOT usually required, but in cases where it is indicated use: Ciprofloxacin
250mg bd po
Pneumocystitis prophylaxis
Co-trimoxazole 960mg od
Treatment of pyrexia episodes in neutropenic patients (Refer to “Trust Policy for the Care of
Neutropenic/ Immunocompromised Patients)
 Temperature >39O C on one occasion OR
 Temperature > 38O C on 2 occasions OR
 Rigor OR
 Hypotension +37.5 OC OR
 Other signs of sepsis.
Treatment:
 Tazocin® 4.5g tds IV and
 Gentamicin# 5mg/kg IV (single daily dose regimen) Max 480mg
If MRSA colonised or suspected consider:
 Vancomycin *1g od IV (or Teicoplanin 400mg bd IV for 3 doses then 400mg od thereafter)
Line-associate septicaemia (peripheral and central cannulae, Hickman line)
 Vancomycin* 1g bd IV
Peripheral cannulaassociated soft tissue infections without sepsis
 Flucloxacillin 500mg qds po for 7 days
Helicobacter pylori eradication
 Lansoprazole 30mg bd po and
 Amoxicillin 1g bd po (in penicillin allergy, Metronidazole 400 mg bd and
 Clarithromycin 500mg bd po for 7 days
Catheter associated bacteriuria
 Urine dipsticks are unreliable for catheter urine.
 Antibiotics are NOT required unless the patient is systemically unwell.
 Send CSU if patient systemically unwell. Treat according to culture and consider remove/change
catheter.
Moderately severe UTI
 Co-amoxiclav 1.2g tds IV for 5 days (3 days in women) unless MSU indicates otherwise or if
infection not resolving.or
 Gentamicin# 5mg/kg IV (single daily dose regimen) Max 480mg in penicillin allergy
Severe UTI and/or acute pyelonephritis (acute pyelonephritis will require 7-10 days treatment in total)
 Gentamicin# 5mg/kg IV (single daily dose regimen) Max 480mg. Review after 48 hours and step
down to oral therapy as for mild uncomplicated UTI
 Tazocin® 4.5g tds IV (if Gentamicin contraindicated) Review after 48 hours and step down to oral
therapy as for mild uncomplicated UTI
 If Gentamicin contraindicated in penicillin allergic patients and carbapenems tolerated use
Meropenem 500mg tds -1g tds IV.
 If neither gentamicin or meropenem appropriate consider Ciprofloxacin 500mg bd po
Periorbital cellulitis
Organisms other than staphs and streps, such as Haemophilus can cause this serious infection hence the
need to consider Cephalosporins and for quinolones if benefit is felt to outweigh risk


Benzylpenicillin 1.2-2.4g qds IV AND Flucloxacillin 1-2g qds IV
OR
Ceftriaxone 2g od and Metronidazole 500mg IV tds (400 mg po tds) if severe and spreading.

Review after 48 hours and modify according to progress + organisms isolated
In penicillin allergic patients Vancomycin* 1g IV twice daily plus Ciprofloxacin 200mg bd IV and metronidazole 500mg tds IV if
severe and spreading
 Review after 48 hours and modify according to progress + organisms isolated, and consider oral
therapy:



Fever
Hypotension,
Clarithromycin 500mg bd po for 7 days then review
Diabetes Related Foot Infection: criteria for admission
Severe – Borderline admission
Cellulitis >2cm around the ulcer associated with;
 Lymphangitis
 Foot failing to respond to oral antibiotics alone
Severe – Admission
Cellulits as well as features of systemic toxicity:
 Leukocytosis
 Hypotension
 Fever
Or
 Abscess formation
 Lymphangitis
 Wet gangrene
 Failure of antibiotics
Alcohol withdrawal
Signs and symptoms of alcohol withdrawal can appear any time between 6 and 72 hours after last
alcohol use.
Delirium tremens (DTs) occurs usually 2-5 days after alcohol cessation or decreased intake. DTs is fatal
in 15-20% of inappropriately managed patients,
It is characterised by:

Increasing confusion and disorientation

Severe tremor and autonomic disturbance

Visual and auditory hallucinations

Delusional beliefs
Wernicke’s Encephalopathy (WE) may develop rapidly or in a couple of days.
WE is initially reversible with parenteral Vitamin B. It carries a mortality rate of 15% and can result in
permanent brain damage
The classical triad of signs (acute confusion, ataxia and ophthalmoplegia) occurs in only 10% of patients.
Therefore, the triad cannot be used as the basis of diagnosis. The presence of only one of the signs
should be sufficient to assign a diagnosis and commence treatment.
In general longer acting benzodiazepines (such as Chlordiazepoxide) are more effective in reducing
seizures, and allow a smoother withdrawal with less rebound
0.5 mg lorazepam = 5 mg diazepam = 10-15 mg Chlordiazepoxide
Acute Compartment Syndrome in adults
The end result of unchecked ACS includes neurological deficit, muscle necrosis, ischaemic
contracture, infection and delayed fracture healing.
Irreversible damage can also lead to amputation, renal failure and even loss of life (Appendix 3).
The diagnosis of ACS has been based on
 The detection of clinical signs and symptoms and routine monitoring of the extremities
for neurovascular status
 EXTREME PAIN (on passive stretch/out of proportion to injury)
 Continuous compartment pressure monitoring. All patients who have sustained
diaphyseal tibial fractures or who are deemed at risk of developing ACS, are to have
compartment pressure monitoring via continuous compartment pressure monitoring.
Causes:
A Fracture or contusion
 Most common cause
Soft tissue trauma
 Not to be excluded
Constriction and external compression
 Unconscious patients following anaesthesia or alcohol/substance misuse leading to
entrapment of the limb
 Entrapment of the limb under a heavy load
 Prolonged inflation of air splints
 Incorrect application of circumferential casts (POP, Scotchcast™)
Revascularisation

Post-ischaemic swelling after circulation restored following vascular reconstruction particularly if restoration of the circulation is delayed > 6hours
Surgical procedures with elevation of the lower limbs
 e.g. Lloyd Davies/Lithotomy position for > 4 hours
Thermal Injuries
 Circumferential burns
 Electrical burns (raised interstitial pressure resulting from associated oedema)
Intravenous extravasation
 Occlusion or spasm of a major vessel with an inadequate collateral circulation can also
cause swelling of the contents to a muscle group
 Patients taking anticoagulants or with bleeding disorders are at greater risk
Signs and Symptoms – The 6 ‘P’s
Pain
 Out of proportion to the injury
 Unrelieved by narcotics
 Excessive use of analgesic devices (PCA)
 Increases with elevation of the extremity
 May not be present if central/peripheral sensory deficits are present
Parasthesia
 Subtle first symptom
 Best elicited by direct stimulation
 Patient complains of tingling or burning sensation
 Can lead to hypoesthesia (numbness)
Pressure
 Involved compartment or limb will feel tense and warm on palpation
 Skin will be tight and shiny
 Skin occasionally appears cellulitic
Pallor
 Prolonged capillary refill - > 3 seconds
 Cool feel to skin due to lack of capillary reperfusion
Paralysis
Pulselessness
ACS - Important Points to Remember
Parasthesia/hyperparasthesia (Sensory changes in the nerve)
 Develop within 30 minutes of the onset of ischemia
Irreversible functional changes
 Start in the muscle after 4 hours
Irreversible nerve damage
 Begins after 12/24 hours of total ischaemia
Fracture blisters

Represent areas of necrosis of the epidermis and separation of the skin layers
 Often occur in areas of swollen skin over a fracture site. When the intracompartmental
pressure is too high to be relieved by normal physiological means, blisters occur as the
body attempts to relieve the pressure
 Associated swelling must be noted as a sign of significant interstitial pressure
Elevation
 Too high - can contribute to the risk
 Should not be above the level of the heart
Renal Failure

All patients are at risk of renal failure
 Monitor renal function and urine output regularly
Patient Information Sheet
 Enables patient to recognise early symptoms
 Enables patient to alert nursing staff of any symptoms
Recordings:
The diastolic blood pressure and the compartment pressures are recorded HOURLY on the
compartment pressure monitoring form. Differential Pressure (P). should be above 30mmHg
to be considered within normal range. If the P falls below 30mmHg for two consecutive
readings, the SHO/SPR should be informed. A falling trend signifies the onset of ACS and
early return to theatre for Fasciotomy is desirable. The monitor remains in situ for 48 hours post
fixation/pre POP if non-operative treatment.
Adult Patients requiring Anticoagulation with Warfarin
VTE (DVT and/or PE) - based on BCSH recommendations (2005 update of guidelines
on oral anticoagulation (3rd edition)
Indication
Target INR
Minimum duration
Calf – irrespective of risk factor
2.5
6/52
proximal DVT or PE – temporary
2.5
3/12
risk factor
proximal DVT or PE - idiopathic
2.5
at least 6/12
or permanent risk factor
VTE associated with
2.5
while disease active
Antiphospholipid syndrome
? lifelong
Recurrence of VTE while on
3.5
lifelong
Warfarin in therapeutic range
Recurrence of VTE after
2.5
review for permanent risk
cessation of warfarin
factors ? lifelong
Cancer with VTE
2.5 consideration for
while cancer active
therapeutic LMWH as an
alternative
Cardiac Indications for valve replacements
Indication
Target INR
Atrial Fibrillation
2.5
Cardioversion
Mural thrombus
Mechanical Mitral valve
Mechanical Aortic valve
Bioprosthetic (tissue) valve
Other
Indication
Arterial thrombosis associated
with anti-phospholipid syndrome
Peripheral arterial thrombosis
and grafts
Paroxysmal Nocturnal
Haemoglobinuria
2.5
2.5
3.0
2.5
None unless specified
Target INR
2.5 –3.5
antiplatelet drugs first line
if given – 2.5
If clones >50% blood
mononuclear cells and
platelets >100 x109/L
target 2.5.
Consider for smaller
clones and lower platelet
counts if other risk factors
and risks of thrombosis >
bleeding.
Minimum duration
Lifelong unless for
cardioversion
Should be in therapeutic
range (2-3) for at least 4
wks before and 4 weeks
after cardioversion
3/12
lifelong
lifelong
None unless specified
Minimum duration
while disease active
? lifelong
long term
long term
Patient overanticoagulated
INR too high but <8, NOT bleeding (if major bleeding intracranial, intraocular, compartment
syndrome, haemorrhage with hypovolaemic shock, pericardial
INR
omit Warfarin
days
3.1-3.5
0
3.6-4.0
0
4.1-5.0
1 day
5.1-6.0
6.1-7.9
at least 1
at least 2
Repeat INR
Suggested % dose
reduction
at 2 days unless clinically indicated e.g.
active bleeding or medically unstable
at 2 days unless clinically indicated e.g.
active bleeding or medically unstable
at 2 days unless clinically indicated e.g.
active bleeding or medically unstable
daily restart Warfarin once INR <5
daily restart Warfarin once INR <5
once Warfarin restarted*
15
20
25
25
33
INR >8 or major bleeding
INR
INR >8.0, no bleeding or minor
bleeding
Action







Major bleeding - defined as
haemorrhage with hypovolaemic
shock
or bleeding into a confined space  intracranial
 intraocular
 compartment syndrome
 pericardial
irrespective of INR
Contact consultant
haematologist (tel 6744 9-5, Mon
to Fri; via switchboard
otherwise)
Contact consultant cardiologist
if patient has a mechanical
prosthetic heart valve






stop Warfarin
give 2mg of phytomenadione orally (use iv Konakion MM
preparation orally)
recheck INR daily
try to identify precipitating cause - is it temporary e.g. drug
or permanent e.g. liver failure?
if INR still >8 at 24 hours consider repeating dose of
phytomenadione
when INR <5, review need for anticoagulation
restart Warfarin if appropriate at reduced dose - 50% of
previous dose
stop Warfarin
urgent clinical assessment
urgent clotting screen
give 5mg phytomenadione iv
give Beriplex 30IU/kg by slow iv injection – max rate 210
IU/min generally over 10 mins (obtained from Blood bank)
check clotting screen 1 hr after administration
inadequate correction – consider other causes e.g. DIC;
discuss with consultant haematologist consider second dose of
Beriplex 20 IU/Kg



recheck INR within 24 hours and daily thereafter
a source of bleeding should be looked for
both Beriplex and phytomenadione may need to be
repeated if bleeding continues/INR rises/complete reversal
of Warfarin is required


when INR <5, review need for anticoagulation
restart Warfarin if appropriate at reduced dose - 50% of
previous dose
Notes
 patients with mechanical prosthetic heart valves should be discussed with a consultant
cardiologist
 some patients who require interruption of anticoagulation may require insertion of
temporary filter (see Trust guideline on VC filters) e.g. with very recent PE who require
emergency surgery
 all patients should have their indications for anticoagulation reviewed prior to
restarting warfarin and the risks of thrombosis versus further bleeding assessed
 incident forms should be completed for patients who develop INRs > 8 while
hospital in-patients or who are admitted to hospital as a result of
overanticoagulation
Beriplex









must be discussed with consultant haematologist before use
is NOT a substitute for FFP in situations of massive haemorrhage where all
coagulation factors may be reduced
is a Prothrombin complex concentrate (PCC) derived from human plasma which has
been virally inactivated
contains coagulation factors II, VII, IX and X but no other coagulation factors
is kept in Blood Bank as a freeze-dried powder which is reconstituted with a small
volume of water just prior to use
is given by slow iv injection maximum rate 210 IU/min generally over 10 mins
it is NOT useful in patients whose INRs are prolonged for reasons other than warfarin/
coumarin treatment e.g. liver disease
doses given are based on the dose of administered factor IX
vial contains 500IU factor IX
Indications

patients to be considered:
o recent abrupt intracranial haemorrhage, preferably demonstrated on CT scan;
patient expected to survive 24hr
o haemorrhage with hypovolaemic shock (remember all coagulation factors may
eventually decline and FFP may be required)
o intraocular bleeding
o muscle bleed with compartment syndrome
o patients requiring emergency surgery who are anticoagulated with warfarin
Contraindication
o
o
relatively contraindicated in patients with venous thromboembolism within last
month as Beriplex is thrombogenic. You may need to consider placement of
inferior venal caval filter in these patients (see Trust guideline CA2101 Insertion
of Vena Cava Filters)
contraindicated in patients known to be allergic to Beriplex
Possible side effects
o
o
o
may cause thrombosis
allergic reactions
plasma derived product so risk of infection must be borne in mind
Surgical patients on Warfarin

emergency surgery requiring reversal within 1hr – give Prothrombin Complex
Concentrate Beriplex 30IU/kg (see Beriplex section E) check INR pre operatively

emergency surgery requiring reversal in 4 to 48 hr – give phytomenadione 5
mg by slow iv injection; check INR ≤ 6 hours pre operatively
On discharge all patients should have



counselling regarding the risks and benefits of anticoagulation with Warfarin
the DoH yellow anticoagulant therapy record with patient details completed and the
contents explained to patient
arrangements must be made for subsequent monitoring of the INR
Control of Chemotherapy and Radiotherapy Induced Nausea and Vomiting in Adults



Ondansetron 8mg po bd 3/7
Dexamethasone 4mg po bd 3/7
Domperidone 10-20mg po qds prn
Extra pyramidal reactions - may occur (rarely) with metoclopramide, levomepromazine and
prochlorperazine; consider stopping causing drug or switching metoclopramide to domperidone (which
causes fewer side effects).
Treatment - Procyclidine 5 mg iv (usually effective within 5 mins)
Long Lines
Long lines are small gauge silastic or polyurethane catheters, which are inserted into a peripheral vein
and advanced to a central position, ideally in the inferior or superior vena cava, lying outside the heart.
Indications
� Administration of parenteral nutrition.
� Long term administration of intravenous medication.
� Administration of inotropes.
� Administration of hyperosmolar fluids or irritant drugs
� Limited intravenous access
Notes
In cases of recent sepsis wait at least 24 hours after removal of previously infected lines
if possible.
Consider the infants’ comfort during the procedure - analgesia, anaesthetic creams or
comfort measures
The catheter tip position must be verified with an x-ray (plus contrast if PACS does not
confirm position tip)
The ideal position is the superior vena cava atrial junction or in the inferior vena cava
1
at the level of the diaphragm
Looped catheters must be withdrawn as there is a risk of migration
In any infant who collapses with a long line in situ, it is critical to urgently exclude cardiac
tamponade as a cause of the collapse.
1
Insertion sites
Antecubital veins- basilic and cephalic veins
Saphenous veins
Scalp veins - temporal and posterior auricular veins
Occasionally:
Axillary vein
External jugular vein
Femoral vein
Complications
 Malposition from outset
This is identified by the x-ray taken after insertion.
 Infection
 Catheter migration
� The catheter may have looped during dwell time or on insertion.
� May migrate to the cardiac chambers, internal jugular vein, subclavian vein, ascending lumbar
vein.
� Can cause pericardial effusion, pleural effusion, cardiac arrhythmias , tamponade, or cardiac
perforation and tissue extravasation
Consider pericardial effusion/cardiac tamponade in any neonate who collapses with a long
line/central venous catheter
 Catheter Dysfunction
� Indicated by a rise in the pressures or inability to infuse fluid
� Due to malposition, fibrin clot, precipitate from infusate with high mineral content, drugs or lipid
deposits.
� Flexion of an extremity may also lead to temporary occlusion
14


Catheter Breakage
Tethered Catheter
Difficulty in removing the catheter due to the formation of a fibrin clot especially
when multiple attempts are made at insertion
Other Complications:
� Thrombosis (renal, intracardiac, deep vein)
� Pulmonary embolism
� Air embolism
Damage to other vessels:
� Pneumothorax
� Puncture of the subclavian artery
� Pneumomediastinum
CHICKENPOX AND PREGNANCY
It may cause maternal mortality or serious morbidity. It may also cause fetal varicella
syndrome.
The incubation period is 10-21 days and the disease is infectious 48 hours before the rash appears
and until the last vesicles have crusted over.
Immunity is checked by sero-positivity for VZV immunoglobulin G (Ig G) antibody
Complications:
Pneumonia, Hepatitis and encephalitis
MANAGEMENT OF SUSPECTED VARICELLA CONTACT IN PREGNANCY
Three aspects of exposure should be ascertained:1. The type of VZV infection in the index case – the risk of acquiring infection from an
immune-competent person with non-exposed chickenpox or zoster lesions (ie. all lesions
covered by clothing), is remote.
Exposure to
a) uncovered chickenpox lesions,
b) disseminated zoster or
c) localised zoster on any part of the body of an immunocompromised patient is a
significant risk to a pregnant woman or neonate.
2. Timing of exposure in relation to onset of the rash in the index case
a) In chickenpox or disseminated zoster the risk is significant between 48 hours prior to
rash onset until crusting of the lesions.
b) In localised zoster, the index case is infective from the day of onset until crusting of
the lesions.
3. Closeness and duration of contact - face-to-face contact during a conversation and
contact within the same room for more than 15 minutes would constitute a significant
exposure (risk of infection is remote if lesions covered).
If there is a definite history of chickenpox in the pregnant woman, it is reasonable to assume
immunity.
Page 75 of 113
If there is any doubt about the immune status, serum should be tested for VZV IgG. Contact
Microbiology department, NNUH (telephone number 01603 611816 or N.N.U.H. extension
4588) who may be able to use the serum stored from the booking antenatal bloods. At least
80-90% of women tested will have VZV IgG and can be reassured.
If a pregnant woman is susceptible to VZV and she has had a significant exposure to
chickenpox, she should receive VZIG regardless of the stage of pregnancy (available from
Microbiology Department) within 10 days of contact. VZIG may not prevent but may
attenuate the infection if given up to 10 days after exposure. There is no benefit in
administering VZIG >10 days after contact but prophylactic aciclovir may be considered,
after discussion with a consultant.
MANAGEMENT OF THE PREGNANT WOMAN WHO DEVELOPS CHICKENPOX
General
They should avoid contact with other pregnant women and neonates until at least five days after the
onset of the rash or until all the lesions have crusted over.
Oral aciclovir, given within 24 hours of onset, reduces the duration of fever and
symptomatology of varicella infection but is not licensed for use in pregnancy. The UK
Advisory Group on Chickenpox recommends that oral aciclovir should be considered, after
discussion with a consultant, for women with chickenpox if they present within 24 hours of
developing the rash. The dose is 800mg five times a day for 7 days.
Indications for referral to hospital include:
 development of chest symptoms
 neurological symptoms
 haemorrhagic rash or bleeding
 a dense rash with or without mucosal lesions
Delivery during the viraemic period may be very hazardous. The maternal risks include bleeding,
thrombocytopenia, D.I.C. and hepatitis. There is also a high risk of varicella of the newborn with
significant morbidity and mortality. Admission under a physician may be more appropriate with close
liason with the obstetric team.
RISK TO NEONATE IF A SIBLING HAS CHICKENPOX
If there is contact with chickenpox in the first 7 days of life and the mother is immune, the risk
to a neonate born at term is minimal because it is protected by passively acquired maternal
antibodies. No intervention is required.
However, in the following circumstances the infant should receive VZIG:




if the mother is not immune to VZV
if the neonate delivered before 28 weeks, regardless of maternal history. Sero-testing of the
premature infant should be attempted if there is a maternal history of VZV.
If the infant weighs less than 1kg
If the infant is known or suspected to be immuno-compromised by disease or treatment eg.
steroid therapy
. Major differential diagnoses of the child with a limp and typical features
Condition
Typical features
Septic arthritis (hip or
other joint)
Any age. Most common <2yrs. Very painful
(pseudo-paralysis). Often non-weight bearing.
Fever and unwell
Osteomyelitis
As septic arthritis but often more indolent
presentation. Partial treatment with antibiotics
common
Irritable hip syndrome
4-10 years. Post viral. Pain and limp
Fracture – nonaccidental injury or
unrecognised trauma
Take history carefully. Be alert to late presentations,
inconsistencies. Special consideration to fractured
fibula
Inflammatory arthritis
(reactive, JIA, lyme
disease, HSP)
Definite joint swelling (not detectable in hip but seen
in other joints). Decreased ROM but not as painful
as septic arthritis. Longer history. Morning stiffness
/ pain after period of rest
Late presentation of
Developmental
Dysplasia
Delayed walking, always walked with limp.
Asymmetrical skin creases, shortened leg, limitation
of abduction in flexion.
Perthes disease
4-10 years, boys>girls. Limp, groin, thigh or knee
pain. Internal rotation of hip often reduced first.
Slipped upper femoral
epiphysis
8-15yrs boys>girls. Longer history limp, sudden
minor trauma often worsens pain and leads to
presentation, knee pain
Neoplasia (leukaemia,
osteosarcoma etc.)
Night pain. General malaise. Weight loss, hepatospleno megally / pallor/ bruising
HSP- Henoch Schönlein purpura, JIA – Juvenile idiopathic arthritis, ROM – range of
movement
Assessment
Initial assessment and documentation:
Pain - assess on pain scales according to age. Give appropriate analgesia
Temp, pulse, resps.
Weight (height if able)
Medical assessment:
B. Key points of history
 A history of preceding viral symptoms is often found in irritable hip.
 Preceding streptococcal sore throat / diarrhoeal illness in reactive arthritis
 Fever height, duration, frequency
 Recent antibiotic use may mask or partially treat a septic arthritis /
osteomyelitis
 Is the child generally well or unwell? Is s/he eating and drinking normally
C. Examination key points
 Is the child generally well or ill?
 Gait and are they able to weight bear?
 Observe, palpate and move all bones and joints (erythema, swelling,
restriction, pain)
 Severity of pain?
 Temperature?
In Septic arthritis or osteomyelitis please try to obtain synovial fluid or tissue
biopsy before commencing antibiotics to ensure organism and sensitivities known.
All children < 2 years
This age group are difficult to assess. Sudden onset of non- weight bearing or limp is
highly unlikely to be irritable hip and may include all the above differential diagnoses
(except Perthes or SUFE).
Careful and full examination is imperative if clues concerning non-accidental injury,
osteomyelitis and septic arthritis at any site or inflammatory arthritis are to be
detected. Fully expose, palpate and move all bones / joints. Ensure full general
examination is done including ENT and urine dip if febrile. Consider haemarthroses
in child with excessive bruising. Developmental dysplasia of hip may present late with
limp in first walking toddler.
X-Ray affected bones / joints (or whole of lower limb if very difficult to localise
problem). If a fracture is present consider mechanism and any child protection
issues. Refer to orthopaedics for fracture management.
If no fracture, consider differential diagnosis and request blood tests accordingly
(FBC, ESR, CRP, Blood culture as a minimum). Request ASOtitre, anti-DNAse B and
viral serology if reactive arthritis likely. ANA, autoantibody screen, immunoglobulins
and rheumatoid factor are indicated if arthritis is likely but are not required urgently,
or at first presentation.
Children 2-9 years
This is the commonest age group for irritable hip. The key is not to miss children with
a septic hip joint since severe destruction of the joint can occur within 24 hours if not
treated.
If any doubt, investigate with blood tests and consider USS and aspiration /
observation / admission / orthopaedic opinion. If Perthes is seen on X-ray refer to Mr
Tucker.
All children > 9 years
Request AP and frog leg lateral hip X-ray to look for SUFE or Perthes
Child with non-blanching rash
No single clinical feature is discriminating.
High risk clinical features:
 Listlessness and lethargy
 Irritability



Shock, prolonged capillary refill time &/or hypotension
Purpura (non-blanching leasion) >2mm diameter
Neck rigidity
Distribution of the rash:
 In the absence of high risk clinical features, the distribution of the rash is helpful.
 If the lesions are largely confined to limbs (particularly lower limbs and buttocks),
urticarial at onset and progression to purpura then a diagnosis of HSP should be
considered.
 If the lesions are petechial and restricted to the distribution of the SVC, sepsis is
extremely unlikely. If no high risk features are present, patient can be discharged.
Parents ahould be given information on the symptoms and signs of sepsis and instructed to
return if such features develop.
Investigations:
FBC
CRP
Clotting studies
Blood culture
If the results (WBC, neutrophil, CRP, and INR) are within normal limits, the patient may be
discharged. Patients with abnormal values for any of these should be managed as
meningococcal disease.
Diabetic Keto-acidosis:
DIAGNOSIS
Characteristic
Known to have diabetes?
Duration of symptoms
Blood glucose (mmol/L)
Ketones in urine or blood?
pH
Bicarbonate (mmol/L)
DKA
Usually yes
Hours or days
>14
Yes
<7.3
<15
HHS / HONK
Not as often
Often days
>33
Usually no
Usually normal
Usually normal
1. DKA usually presents in someone who is known to have type 1 diabetes. HONK may be the first
presentation of type 2 diabetes
2. Vomiting is common in DKA, but abdominal pain is sometime present – always perform a blood
glucose on someone presenting with abdominal pain or unexplained vomiting. Operating on a
patient with untreated DKA is almost always fatal.
Call HDU / ITU if the patient is seriously ill
 pH<7.2,
 Base Excess >-12,
 GCS ≤ 9
 oliguria, renal cardiac failure or other significant co-morbidity)
 If GCS ≤ 8 then patient should be intubated and ventilated
FIRST STEPS –
1. Airway - 35% oxygen via mask. If GCS ≤ 8 then patient should be intubated and ventilated.
2. Establish 14 or 16 gauge peripheral intravenous access. If this is not possible due to the clinical
state of the patient, central venous access may be necessary. Call HDU.
A CVP LINE IS ADVISABLE IF THE PATIENT HAS A HISTORY OF CARDIAC FAILURE OR RENAL
IMPAIRMENT (CREATININE >150 μmol/L), OR IS NOT CLINICALLY IMPROVING AFTER INITIAL FLUID
RESUSITATION
3. Measure arterial blood gases on admission
4. Obtain venous blood for U&E’s, LFT’s, glucose, FBC, osmolality, blood ketones, and blood cultures
5. Give 1 litre of 0.9% Sodium Chloride stat
6. Give 10 IU of human Actrapid insulin intravenously (or IM if there is a delay in setting up the IV
infusion) then set up an insulin infusion
7. Start intravenous Actrapid insulin at a constant rate of 6 IU/hr.
SECOND STEPS –
1. Naso-gastric tube if conscious level is depressed or the patient is vomiting. If no gag reflex refer
to HDU
2. Insert a urinary catheter if conscious level is depressed or the patient is oliguric
3. Subcutaneous Low Molecular Weight heparin. This should be therapeutic dose in HONK, and
prophylactic dose in DKA
4. ECG and continuous cardiac monitoring is essential in all patients where there is a potential for
significant electrolyte swings, and where a cardiac precipitant is possible.
5. Look for a precipitant – e.g. MI, CVA, chest or urinary infection, the acute abdomen
6. Chest X-Ray
7. Intravenous broad spectrum antibiotics if the patient is pyrexial and / or severely ill
Fluids: Normal saline or Hartmann’s if Sodium<155 mmol/l. If the sodium level is >155 mmol/l they
should be considered for HDU - 1st Litre stat, 2nd Litre over 60 minutes, 3rd Litre over 2 hours
Potassium:
Aim for levels between 4 and 5 mmol/Lby adjusting the KCL concentration in each bag of fluid.
Initially use normal saline with 20 mmol/L KCL. However:
If K+ < 4.0 mmol/L, then use 40 mmol/L in each litre of 0.9% sodium chloride or glucose
If K+ >5.0 mmol/L, use 0.9% sodium chloride only or glucose only, without K+
Bicarbonate
Highly controversial. It should be considered if the pH is < 7.0, remembering that it can cause a
precipitous drop in the potassium level. If bicarbonate is being considered, the patient MUST be on
HDU / ITU for monitoring. Lesser degrees of acidosis can be adequately treated with fluids and
insulin alone.
PROBLEMS
1. If conscious level deteriorates with treatment, consider cerebral oedema or an
intracranial event. Acute cerebral oedema is rare in people over 20 years old, and is
associated with the use of artificial ventilation and bicarbonate infusion. Refer to ITU
/ HDU.
2. As mentioned above, DKA can cause abdominal pain. However, if the patient has
a bicarbonate level of > 15 mmol/L and still has abdominal pain, ask for a surgical
opinion.
3. DKA is associated with leukocytosis (without sepsis), increased creatinine levels
(ketones interfere with the assay) and increased amylase (of salivary origin NOT
pancreatitis)
4. Remember: overdoses of aspirin, alcohol or ethylene glycol can mimic DKA and
should be born in mind if the presentation is atypical.
Diabetic Keto-acidosis in children
DKA is characterised by:
 Unwell child with clinical features of dehydration
 Hyperglycaemia (Glucose >11.0mmol/l)
 Elevated blood ketones (>3.0mmol/l on ward test) or Heavy ketonuria (3+ or
4+)
 Acidosis (pH <7.35, HCO3 <15mmol/l)
Why important





Diabetic Ketoacidosis is an emergency.
Scrupulous attention to fluid and insulin management is essential
Cerebral oedema is the principal cause of death and disability. Other causes
include aspiration and cardiac arrhythmias.
Children requiring large volumes of fluid resuscitation (greater than 40ml/kg)
usually require transfer to a paediatric intensive care unit.
These measures have been shown to improve outcome.
Immediate Management steps





It is essential to monitor Airways, Breathing & Circulation, and to frequently reassess the
child.
Initial assessment and diagnosis
Shock management
Fluid & Insulin administration
Monitoring

Recommendations for transfer to a Paediatric Intensive Care Unit. Children with
Decompensated Shock, or who are very young (<3y), or who require greater than
40ml/kg of fluid resuscitation usually require Paediatric Intensive Care
Risk factors for cerebral oedema include
 young age (<5y),
 severe acidosis,
 hypocapnia, elevated urea at presentation,
 large amounts of fluid resuscitation (>40ml/kg),
 use of bicarbonate and
 overly rapid fall in blood glucose.
Fluid replacement is based on maintenance + correction for dehydration.
Shock is corrected by the boluses of 20 ml/kg of normal saline.
Maintenance fluid rate is calculated from body weight (Kg)
 100ml/kg/day or 4ml/kg/hr for first 10kg body weight
 50ml/kg/day or 2ml/kg/hour for each kg between 10 and 20kg
 20ml/kg/day or 1ml/kg/hour for each kg above 20kg
 Example: Child of 23kg admitted with DKA:Maintenance calculation


[10x100] +[10x50] + [3x20] = 1560ml/day = 65ml/hr

Percentage dehydration is based on clinical estimate or a recent clinic weight. It is easy to
over-estimate % dehydration in DKA, therefore NEVER assume dehydration exceeds 10%.
The correction for dehydration is administered over 48 hours.
Example: Child of 23kg admitted with DKA
Estimated % dehydration is 5%, therefore deficit = 0.05 x 23 = 1.15 litres (1150ml), given
over 48 hours – ie 575ml/day + maintenance.
Administer insulin at 0.1u/kg/hour. Adjust iv fluids to maintain glucose at adequate levels.
Insulin may be reduced to 0.05u/kg/hr if: a rapid reduction in glucose occurs (>5mmol/hr),
particularly in young children. Or Blood glucose is persistently below 7.0mmol/l, despite
using 10% glucose
Fluids Used:
 If glucose >13mmol/l, use 0.9% (“Normal”) Sodium chloride
 If glucose between 7.0 and 12.9mmol/l, use 0.45% Sodium chloride with 5% glucose
unless hyponatraemic (Na <132mmol/l)
 If glucose between 7.0 and 12.9mmol/l with hyponatraemia, use 0.9% Sodium chloride
with 5% Glucose.
All children require ¼ - ½ hourly neurological observations until stable when the frequency
may be reduced. These may be discontinued when the child is completely alert and stable.
Children with a depressed level of consciousness require a nasogastric tube. Children with
DKA are at high risk of aspiration, particularly if there is significant depression of
consciousness
Cerebral oedema is a rare and serious complication of treatment of DKA. Morbidity and
mortality is high. If suspected,
 remember ABC and give
 Mannitol 0.5g/kg [2.5ml/kg 20% Mannitol] immediately


Call ICU anaesthetic registrar and notify paediatric consultant
Reduce fluid replacement to 2/3 maintenance only – with no correction for dehydration

Children with cerebral oedema require intubation, ventilation and urgent transfer to a
paediatric intensive care unit
DKA is associated with a potassium deficit, irrespective of the initial plasma potassium.
Once urine has been passed, commence potassium replacement:
Potassium Chloride (KCl) 40mmol/l (20mmol in 500ml bag)
Use of sodium bicarbonate is potentially extremely hazardous, and increases the risk of
cerebral oedema. Use may be justified by severe acidosis with shock, (arterial pH < 7.0, HCO3
< 5mmol/l), to improve myocardial function.
When bicarbonate therapy is under consideration, an arterial blood gas sample is essential
to confirm pH.
When bicarbonate is required, use 1-2mmol/kg over 1-2 hours [1-2ml/kg 8.4% NaHCO3
diluted with an equal volume of normal sodium chloride
Nephrotic syndrome
Diagnosis: Heavy proteinuria, hypoproteinaemia and oedema. Oedema,
which may be peri-orbital (often thought to be allergic initially) or
generalised.
Decreased urine output. Abdominal pain. Ascites, pleural effusions and
genital oedema may occur. Some children may present with hypotension and
dyspnoea.
2-6 years of age most commonly.
Investigations
Urinalysis and culture
Heavy proteinuria (3-4+ on albustix).
Early morning urine protein / creatinine ratio. >200
with nephrotic syndrome.
mg/mmol
in
patients
Blood tests
U&Es, LFTs, FBC, varicella zoster titres.
ASO titre, C3 and C4 components of complement, and antinuclear factor
should be measured in selected cases especially when there is a mixed
nephritic/nephrotic picture. Consider Hepatitis B serology if any risk factors.
Management
During the initial attack attention is focused on management of the
oedematous state and any arising complications until hopefully steroids
induce remission.
a) Volume replacement
Rapid correction of shock or hypovolaemia is essential as per standard
resuscitation guidelines. 20ml/kg of normal saline is the usual
recommendation, but an alternative is 4.5% human albumin solution (HAS)
Hypovolaemia can be associated with sepsis, diarrhoea or the injudicious use
of diuretics.
Hypovolaemia may cause acute tubular necrosis, be complicated by
thromboses (arterial or venous) or lead to sudden death.
Initial treatment with corticosteroids
At presentation a high dose of prednisolone 60 mg/m2/day, (maximum
80mg/day) is accepted practice.
Children with Hydrocephalus and Ventriculo-peritoneal Shunts
Shunt malfunction may be the result of obstruction, infection, disconnection at
the junction or break, hardware erosion through the skin and over shunting.
Shunt evaluation includes ascertaining the reason for initial shunt insertion (e.g.
meningitis, tumour, myelomeningocele)
Assess the Clinical status of the child
ABC
1
Life threatening
symptoms present?
Unconsciousness
Intractable seizures
Unstable vital signs
Dilated pupils
YES
2
3
4
5
NO
6
Are acute symptoms &
signs present?
Headache
Drowsiness
Vomiting
Neck Stiffness
1
YES
2
3
4
NO
Are subacute symptoms
and signs present?
Fever
Irritability
Intermittent Drowsiness
YES
1
2
3
Arrange intubation and ventilation by Anaesthetic
team.
Consider controlling intracranial hypertension
with mannitol (0.5 gram/Kg iv).
For initial advice liaise with Neurosurgeon and
PICU at Addenbrookes hospital.(#6100)
Needle the reservoir to relieve pressure if valve
will not depress.* (send CSF to Microbiology and
Biochemistry).
CT scanning in Norwich is usually inadvisable as
it may delay treatment.
Arrange for transfer once stabilised with CATS
Team (0800 085 0003)
Discuss with and consider transfer to
Neurosurgical Unit at Addenbrookes
Perform CT scan, in Norwich or at the
Neurosurgical centre depending on availability and
consultant advice.
DO NOT GIVE SEDATION for CT scan if any
Impairment of conscious level: transfer to
Neurosurgical centre if sedation / anaesthetic
thought necessary for scanning
Needle the reservoir if present to relieve pressure
if valve will not depress.* (send CSF to
Microbiology and Biochemistry
Consider CT scan in Norwich if previous scans are
available for comparison
Observe carefully (2 hourly Neuro observations)
Consider discussion with the Neurosurgical Unit
drowsiness
NO
If symptoms are mild or resolving consider
discharge home
*Consider needling the reservoir only as
an emergency. Aspirate 10mL/kg/min,
please note that you may not be able to
aspirate with ventricular shunt blockage.
Remember:
A shunt that ‘pumps’ normally can still be blocked.
A normal scan does not exclude shunt malfunction.
If in doubt seek Neurosurgical advice
Indications for red cell transfusion
 acute blood loss (ie>=150mL min-1 or 1 blood volume/24hrs or 50% blood volume
in 3 hours, blood volume is 70mL kg-1 adult, 80mL kg-1 child)






Acute anaemia, fit patient, Hb<7g/dL
Acute anaemia, patient with cardiovascular risks, Hb<9g/dL
Critical care patients, Hb<7g/dL
Post-chemotherapy, Hb<9g/dL
Radiotherapy, Hb<10g/dL
Chronic anaemia, Hb<8g/dL
Indications for the use of fresh frozen plasma
 Replacement of some single coagulation factor deficiencies
 Non-urgent reversal of warfarin effect
 Acute disseminated intravascular coagulation
 As plasma exchange in thrombotic thrombocytopenic purpura
 Massive transfusion and PT >1.5 x control
 Liver disease if PT>1.5 x control
Indications for cryoprecipitate
 in acute disseminated intravascular coagulation with bleeding and fibrinogen
<1g/L
 in advanced liver disease to correct or prevent bleeding with fibrinogen <1g/L
 to correct bleeding in association with fibrinolytic therapy causing
hypofibrinogenaemia
 in massive transfusion associated with hypofibrinogenaemia
 to treat abnormal bleeding in renal or liver failure where desmopressin is
ineffective/unsuitable
Indications for platelet transfusion (refer to full guidance for platelet counts)
In bone marrow failure:
 to prevent bleeding, platelet count<10 x109/L
 to prevent bleeding in patients at increased risk of haemorrhage, platelet count
<20 x109/L
 to prevent bleeding in association with invasive procedures, platelet count <80 x
109/L
In critical care/surgery:
 in massive blood transfusion, platelet count <75 x 109/L
 in bleeding in association with acquired platelet dysfunction, irrespective of
platelet count
 in DIC with bleeding, platelet count <75 x 109/L
 in inherited platelet dysfunction
In immune thrombocytopenia:
 in immune ITP if major significant bleeding
 in post-transfusion purpura only if actively bleeding
 in neonatal alloimmune thrombocytopenia (NAITP) to treat bleeding or to
maintain platelet count >30x109/L
Do not Resuscitate order:
DNACPR status means that in the event of an arrest or collapse the crash team is not
called. Neither advanced nor basic cardiopulmonary resuscitation are given.
This means oxygen and suction may be given, but assisted ventilation using bag and
mask or mouth-to-mouth are not indicated.
This DNACPR order in itself has no other implication for the patient’s management.
Indications for “DNACPR” order :
1
2
3
The child has such severe disease that cardiopulmonary resuscitation would
simply delay death without significant alleviation of suffering.
Although the patient may be able to survive with treatment the degree of
physical or mental impairment would be so great that it is unreasonable to
expect them to bear it.
The child and/or family feel that in the face of progressive and irreversible
illness further treatment or resuscitation is more than can be borne by the
child.
Neonates with murmur
Consider each of these signs

Is the lower limb SaO2 <96%?

Central cyanosis present?

Are there signs of heart failure?
Symptoms & signs of heart failure
 Poor feeding, tired and breathless whilst feeding, takes a long time to
complete feeds
 Tachypnoea, respiratory distress
 Clammy skin, poor perfusion, pallor, cyanosis
 Tachycardia, hyperactive praecordium, gallop rhythm
 Oedema, hepatomegaly
Clinical features suggestive of Congenital Heart Disease
 Symptoms of heart failure
 Cyanosis, SaO2 <96% (pre and/or post-ductal)
 Abnormally strong or weak pulses (Check femoral pulses)
 Praecordial hyperactivity
 Abnormal intensity and character of heart sounds
 Murmur >grade 2/6, harsh
 Diastolic, pansystolic or continuous
 Associated with an ejection click
Henoch – Schönlein Purpura (HSP) in Children
HSP is the commonest vasculitis of childhood.
It is characterised by inflammation of small vessels leading to
 non-thrombocytopenic purpura,
 arthritis/ arthralgia,
 GI haemorrhage and
 glomerulonephritis.
Clinical features
The commonest age group is 2 - 8 years. There may be a recent history of an upper
respiratory tract infection. Abdominal pain or arthralgias sometimes precede the rash.
Purpura: On the extensor surfaces of limbs (mainly lower), or dependent and pressure
bearing areas (ankles / buttocks). Also consult guideline on ‘non-blanching purpuric rash’
Joint Pain: Knees and ankles commonly affected. In most situations this pain resolves
spontaneously within 24-48 hours.
Abdominal pain: Uncomplicated abdominal pain often resolves spontaneously within 72
hours. Complications include GI haemorrhage (haematemesis, bloody stools),
intussusception, perforation, and pancreatitis.
Renal disease: Haematuria is present in 90% of cases, and in up to 40% may recur. Less
common renal manifestations include proteinuria, nephritic/nephrotic syndrome,
isolated hypertension, and renal failure (<1%). Renal involvement may only become
apparent during the convalescent period.
Subcutaneous oedema (scrotum, hands, feet, and sacrum): seen especially in children
<3yrs, can be painful, also resolves spontaneously in 24 - 48hrs.
Investigations



BP in all children
Urine dipstick in all children
U & E – only if renal involvement other than isolated haematuria is suspected.
Include LFT and Albumin if phlebotomy undertaken
Consider prednisolone for: severe GI haemorrhage, severe joint
manifestation, and testicular pain.

If there are features of abdominal complications or painful scrotal
swelling seek a surgical opinion (testicular haemorrhage is difficult to
differentiate from testicular torsion).
Indications for admission:


Abdominal complications
Renal complications (other than isolated hematuria and/or 2+
proteinuria):
Nephritis (persistently elevated BP even after adequate
analgesia, oliguria)
Nephrotic syndrome (oedema, proteinuria, hypoalbuminaemia)
Discuss with consultant. Consider further discussions with Dr
Upton if available or Nottingham renal team (0115 9691169 –
bleep paediatric renal registrar)
Also consider admission for symptomatic treatment of:


Severe joint pain
Severe abdominal pain
Exposure Prone Procedures’ (EPPs)
 “EPPs are those procedures where there is a risk that injury to the worker may result in
exposure of the patient’s open tissues to the blood of the worker. These procedures
include those where the worker’s gloved hands may be in contact with sharp
instruments, needle tips or sharp tissues (spicules of bone or teeth) inside a patient’s
open body cavity, wound or confined anatomical space where the hands or fingertips
may not be completely visible at all times.”

Any HCW who is involved in EPPs and has reason to believe that they have been infected
with Hepatitis C must inform the COH. They will be tested for antibodies to HCV and, if
positive, two specimens of blood for Hepatitis C virus ribonucleic acid (HCV RNA) will be
required two months apart. If positive for HCV RNA, HCWs will be restricted from
performing EPPs. HCV infected HCWs who respond successfully to treatment with anti
viral therapy, i.e. remain HCV RNA negative 6 months after cessation of treatment, may
resume EPPs following advice from the COH. These HCWs will be tested at 6 monthly
intervals.

Any HCW who refuses to be tested will not be allowed to continue undertaking EPPs and
may be subject to disciplinary action if such refusal could adversely affect patient safety.

HCWs that are aware, or have reason to believe that a HCV infected colleague is
practising in a way, which places patients at risk, must report this in confidence to the
COH.

All HCWs must comply with the Trust policy and report all blood/body fluid exposure
incidents to the COH.

Prophylaxis with immunoglobulin or anti-viral agents is not indicated following exposure
to Hepatitis C, as there is no scientific evidence of any benefit.

Where the source patient/individual of an exposure is found to be anti-HCV antibody
positive, the recipient HCW will be offered blood tests to detect seroconversion to HCV.
The COH will provide information and advice on Hepatitis C and its potential impact on
work and lifestyle. It will not normally be necessary to exclude the HCW from
performing EPPs during the period before the results of blood tests are known.
ITP
Take a history of onset of bruising, presence / absence of mucosal bleeding and family
history of bleeding disorder. They are well at presentation. They may have had a viral
infection in preceding 2-3 weeks (50%)
On exam- record purpura, petechiae and echymoses, anaemia, lymphadenopathy,
organomegaly and signs of sepsis. Occasionally nose bleed, melaena or rarely
microscopic haematuria.
Investigations: FBC and Film. No other investigation unless atypical features
All children who receive specific treatment for ITP (steroid or i.v. Ig) should have
evidence of life-threatening heamorrhage.
Patients with Latex allergy : Natural rubber latex (NRL)
“There are 5 possible ways for patients to come into contact with NRL. These are: 
Cutaneous - touching the skin via gloves or other latex products

Mucous membranes - via products used in dental treatment, intubation
and internal examinations and catheterisation.

Intravascular - via latex products used in intravascular devices e.g. IV
cannulae or devices used to deliver IV fluids and injectables (medicine bungs).

Internal tissue - during surgical procedures

Inhalation of glove protein (rare)
Broad Recommendations

The use of latex should be minimised where possible.

Staff is required to follow the Trust guideline regarding the choice of
gloves

staff education

The history of any patients, who are known or suspected to have a latex
allergy, must be passed on as part of their clinical care. This involves liaison
within and outside the Trust.

each area to develop and maintain latex free box/trolley containing
items relevant to the department.

Patients should be nursed in a side room which is clearly labelled
‘Natural Rubber Latex Free’
Identification of patients with Latex allergy
Patient admission assessment must involve a careful history to detect known or possible
occurrence of latex allergy.
Risk Factors
Patients who have a history of any of the following may have an increased risk of
developing a latex allergy:  Spina bifida or other neural tube defects who have required frequent
surgery.
 Atopic individuals especially those with eczema and/or asthma.
 Genito urinary tract abnormalities that have required frequent
catheterisation or surgical intervention.
 Multiple surgical procedures.
 Food allergy in particular bananas, avocados, tomato, kiwi, melon and
mango.
 Those individuals who have occupational exposure to latex, e.g. health
care workers.
A Complete full screening questionnaire with the patient, if they have a documented
positive test or history of allergy/sensitivity or where a latex allergy is suspected following
history taking
When feasible, patients with a suspected latex allergy will be referred by the medical staff
to the Dermatology Department for allergy investigations.
Procedures on all patients with a suspected or positive history of latex allergy should be
performed in a latex free environment.

This is defined as an area where latex gloves are not used by any
personnel, and no latex products of any kind come into direct contact with the
patient.
Emergency or elective procedures and Investigations
At the first point of hospital contact for the patient, it is important to identify latex sensitive
patients. To aid in this:
A screening questionnaire is used.

Latex allergy leaflets

Blood samples may be required for IgE and RAST for latex at the
discretion of the medical staff.

Medical staff should ascertain if the patient is sensitive to latex at the
out patient appointment when the decision is made to proceed with surgery.

When feasible, patients with suspected allergy should be investigated by
referral to the Dermatology Department, especially before medical or surgical
procedures that will entail latex exposure. When urgent treatment is required
this will be undertaken in a latex free environment.

The patient’s G.P. should be contacted with any results or
recommendations.

These should be recorded on PAS and in the patient’s notes.

Patients identified as allergic to latex should receive education in latex
avoidance by the nurse responsible for the patient’s care and should also be
advised to obtain a medical alert bracelet or similar. It may also be appropriate
to advise them to carry a supply of non-latex gloves and to seek advice from
their GP about the necessity of carrying auto -injectable adrenaline (Epi-pens®).
Ward Preparation and Management of Patients’ with known or suspected latex allergy
All should be familiar with:


The preparation of latex free environment
The use of latex free equipment
The management of acute anaphylactic shock
The patient should be allocated a well-ventilated side room, which has been clinically cleaned
by staff wearing latex-free gloves. The need for a side/single room needs to be balanced
with the clinical need of patients currently occupying a single/side room.

All items containing latex should be removed from the room at least two
hours before admission, but preferably the night before.

Aprons and latex free gloves should be available by the door.

Warning signs should be placed at the door (Appendix 4).

The patient should wear a clearly marked patient ID bracelet indicating
LATEX ALLERGIC.

All documentation i.e. medical notes, prescription charts and
observation chart will clearly annotated ‘latex allergic’.

Ensure there are no elastic bands around health records.

Ensure that PAS has been updated with the ALERT status.

The number of clinical staff involved with the patients care should be
restricted to a minimum.

All personnel must wash their hands before entering the room, or
having contact with patients to ensure that they are free of NRL particles.

Intravenous solutions or drugs must not be stored with other NRL
products.

Drugs with NRL seals should not be used.

Syringes should have NRL diaphragms. Two component syringes, minijet system and epi-pens are all NRL free.

Giving sets without NRL ports should be used (or ports removed and
replaced by stopcocks and taped up).

Advice should be sought in hours from the ward Pharmacist or
Medicines Information regarding appropriate medications and their preparation
e.g. latex stoppers on IV drug containers which they are concerned, may contain
NRL (e.g. rubber bungs).

Emergency drugs must always be available to manage anaphylactic
shock i.e. epinephrine, hydrocortisone, chlorphenanime.
Diagnosis of Legionella Infection
Patients at risk:

Patients with severe pneumonia, nosocomially-acquired pneumonia, or significant
immunosuppression

Patients admitted to hospital with radiologically confirmed, community-acquired,
pneumonia and any of the following risk factors:
 Recent travel history
 Middle-age male heavy smoker
 Organ transplant recipient
 Associated with other cases (e.g. place of work)
Suggested testing protocol
On admission
-
Culture of respiratory specimens for legionellae, preferably on
invasive respiratory specimens.e.g.obtained at bronchoscopy.
-
Urine (for antigen detection
Serum to be stored for comparison with later sera.
At one week after admission
-
Test serum in parallel with admission serum. Repeat at weekly
intervals until 4 weeks after onset or until an alternative diagnosis
is established.
N.B.
Urinary antigen
-
antigen may disappear rapidly >5 days after
onset, therefore important to store
admission specimen as routine. Do not
collect in boric acid container.
Causes of scrotal pain:
 infection, (epididymitis, orchitis and epididymorchitis)
 trauma,
 twisting or torsion of the testis,
 torsion of an appendage of the testis,
 idiopathic scrotal oedema,
 incarcerated inguinal hernia and
 Henoch-Schonlein purpura
Urgent scrotal exploration should take place within one hour of a provisional
diagnosis of acute testicular torsion being made
Signs – The child may be in obvious discomfort, have an unusual gait or be reluctant to
move. The scrotal region is usually very tender and may be red and swollen. There may also
be a high riding testicle, absence of cremasteric reflex, a focal blue-dot at the upper pole of
the testis, diffuse blue discoloration of the hemiscrotum or a reactive hydrocele. A high
temperature may also be observed
Investigations
A urine sample should be obtained as soon as possible and a dipstix test performed.
Management
Every boy with acute scrotal pain should be reviewed urgently by a paediatric registrar or
Consultant.
A history of previous transient scrotal pain is significant.
Testicular loss from infarction can occur after as little as 2 hours of onset of symptoms
A delay in treatment can result in orchiectomy, and has been associated with reduced
fertility Thus surgical intervention should ideally take within one hour and acute scrotal pain
should be treated as torsion of the testis until proven otherwise.
Radioisotope scans and Doppler ultrasonography are not part of the initial management of
acute scrotal pain in many centres. This is because it may contribute to delay in treatment
with unacceptable consequences. Moreover, in obese boys and when the testicular volume
is about 2 ml, the diagnostic accuracy of these tests is low resulting in limited clinical benefit.
Special Situations
a.
Where the duration of symptoms is 48 hours or more, the emergency
surgery need not follow the 1 hour rule.
b.
When on examination, the patient has become symptom free and there are
no signs of an acute episode of torsion of testis. If a diagnosis of a spontaneous
detortion / intermittent detortion is made, the testis should be explored as soon as
possible but need not be within 1 hour.
Necrotizing enterocolitis
Clinical features
 Temperature instability
 GI bleeding
 Apnoea
 Lethargy






Pallor
CVS or resp compromise
Abdominal distension
Discolouration / tenderness or abdominal wall oedema
Absent bowel sound
Abdominal mass
Investigations
 FBC, Biochemistry, blood gas
 Group and save, cross match
 Blood and stool culture
 AXR to check perforation, distended bowels, pneumonatosis intestinalis
Risk factores
 Prematurity


Any cause for compromised splanchnic blood flow in the infant, eg maternal
cocaine use,PDA
High osmolarity of formula feed,
Organisms- Klebsiella, staph, E.coli
Treatment
 Stop enteral feeding, NBM
 NG tube and hourly aspiration
 Antibiotics- penicillin, gentamicin, metronidazole
 i.v. fluid- N saline 10 ml/kg, repat
 correct abnormal U&E and glucose and abnormal coagulation
 analgesia- i.v. morphine
 paed surgery referral
Differential diagnoses
 Intestinal perforation
 vovulus
 Umbilical sepsis
 UTI/sepsis
 Ascites
Insertion of umbilical venous catheter (UVC)
1. Goal
To ensure the safe insertion of an umbilical venous catheter
2. Indications
• Venous access for low birth weight infants to avoid multiple
peripheral cannulation
• Emergency vascular access for resuscitation of infants at birth
• Exchange transfusion
3. Contraindications
Abnormalities of the abdominal wall
Necrotising enterocolitis
Peritonitis
4. Complications
2,3
• Sepsis
• Embolism
• Venous thrombosis
• Pericardial effusion
•
•
•
•
4
5
6
Pleural effusion
Portal hypertension
Displacement leading to blood loss
Breakage of catheter on removal
4.1 Malpositioned catheters
• Catheters placed in the heart can cause pericardial effusion, cardiac
tamponade, endocarditis, arrhythmias.
• Catheters placed in the portal system are associated with necrotising
enterocolitis, perforation of colon and hepatic necrosis
5. Key notes
The catheter tip should ideally lie in the inferior vena cava.
The catheter position should always be checked prior to use with an
x-ray
Once secured in place the catheter ideally should not be advanced
into the vein
Do not use hypertonic solutions if the catheter is not in the inferior
vena cava
UVC’s placed during newborn resuscitation should be placed where
there is adequate blood sampling.
Position of the catheter
• Determine the desired length of catheter by calculating 2 x weight
13,14,15
in kg + 5cm + stump length in cms
.
i.e. if infant weighs 1.5kg (1.5 x 2) + 5 = 8cm + stump
• This should place the tip of the catheter above the diaphragm and
outside the chambers of the heart.
CSP - “ Nexus” criteria (National Emergency X-Radiography Utilization
Study Group)
o
o
o
o
GCS 15 and appropriate responses
Absence of alcohol, opiates, intoxicants
No significant distracting injury
No midline tenderness, steps or neurological injury or
impairment to full range of movement of neck.
Recombinant factor VIIa (rFVIIa; Novoseven®, Novo Nordisk)
It is an analogue of the naturally occurring coagulation factor, which is manufactured
by recombinant technology from a cell line and autoactivated during the purification
procedure1. It was developed for use in patients with haemophilia A and B who have
developed inhibitors (antibodies) against FVIII or FIX, respectively. rFVIIa aims to
bypass the missing coagulation factor: supraphysiological doses of rVIIa seem to
enhance thrombin generation on the surface of activated platelets, allowing the
formation of a stable fibrin clot.
Role of recombinant factor VIIa
 Haemophilia care
 Uncontrolled massive bleeding, particularly trauma and obstetric
haemorrhage
 Peri-operative settings
 Intracranial haemorrhage
If rFVIIa is considered, every effort should be made to achieve the following
parameters to ensure maximal effectiveness:
 Platelets >50x109/L
 Fibrinogen >0.5 g/L (ideally >1.0g/L)
 pH >7.2
 Haematocrit >24%
Appropriate blood product replacement:
 FFP 10-15mL/kg: aim INR and APTTr <1.5
 Cryoprecipitate 1-1.5 packs/10kg: aim fibrinogen >0.5g/L, ideally >1.0g/L
 Platelets 1-2 adult doses: aim platelets >50x109/L
 Correct acidosis, hypothermia, hypocalcaemia
Contraindication
Thromboembolic events are the main potential concern with the use of rFVIIa,
because of the possibility of systemic activation of coagulation
rFVIIa should not be used in patients who are considered to be unsalvageable by the
clinical team.
A history of thromboembolic events, coronary artery disease or disseminated
intravascular coagulation should not be considered an absolute contraindication to
the use of rFVIIa, but the clinical team should be aware of the potential for increased
risk of thromboembolic events.
Patients who have received rFVIIa should be monitored clinically for evidence of
thromboembolic events, and should be assessed regularly for appropriate
thromboprophylaxis (compression stockings, and/or low molecular weight heparin
once bleeding has stopped).
Safeguarding Children
 All health service professionals, whether they work within adult services or child
care services, have a responsibility to refer to children’s social care services any
child who they believe is suffering or may be at risk of suffering significant harm.
 Section 11 of the Children Act 2004 places a statutory duty on key people and
bodies to make arrangements to safeguard and promote the welfare of children
 The Trust has a nominated Safeguarding Children team whom staff can consult if
they have concerns or wish to seek general advice.
 A paediatrician, with some exceptions, should be involved if there are concerns
about an immediate risk to a child.
 Although professionals have a duty of confidentiality, in certain circumstances,
the law permits the disclosure of confidential information necessary to safeguard
a child.
 It is the responsibility of the professional identifying the concern to ensure that a
referral to children’s social care services has been made if appropriate and to
access the proper support.
 Parent’s permission should be sought before a referral is made unless permission
seeking may in itself place a child at risk of significant harm.
 All staff have a responsibility to ensure they keep up to date with relevant training.
 Members of staff should also be aware that they should not write reports for case
conferences, court or strategy meetings without first contacting a member of the
Safeguarding Children team, nor should they attend such a conference or court
without the support of the team.
. If any members of the Trust identifies a concern that a child may be at risk there
should be discussion and, if necessary, referral. The initial discussion should
involve the line manager and, if necessary, a member of the Trust Safeguarding
Children team. Further advice can be obtained from the on-call community
paediatrician via switchboard. If, in the light of initial discussions, concerns are
confirmed then the child should be referred. Referrals can be passed to the on-call
paediatric team
Staff are reminded of the importance of keeping safe and avoiding conflict. The
parents or carers should not be confronted.
No attempt should be made to
physically restrain families who are acting against advice and are seeking to leave. If
families leave under these circumstances police and children’s social care services
should be involved as a matter of urgency. If families or carers become threatening
or abusive call security or the police.
GMC guidance
The safety of the child is paramount and overrides the usual duties of confidentiality.
Guidance from the General Medical Council states, ‘If you believe a patient to be a
victim of neglect or physical or sexual abuse and unable to give or withhold consent
to disclosure you should usually give this information to an appropriate responsible
person or statutory agency in order to prevent further harm to the patient. In these
and similar circumstances you may release information without the patient’s consent,
but only if you consider that the patient is unable to give consent and that disclosure
is in the patient’s best interests’.
Scabies in Adults/Children
Scabies mites, Sarcoptes scabiei, burrow in human epidermis digesting it as they go.
They burrow primarily at night and rest to lay eggs during the day.
Although, at standard room conditions, infectious mites can survive for up to 36
hours off the host, there is little risk of transfer of the infestation via clothing,
bedding, towels or upholstery used by patients with typical symptoms of scabies.
However, such transfer is a risk in patients presenting with the less common variant,
crusted scabies (formerly called Norwegian scabies), characterised by heavy
infestation of mites.
Diagnosis of Case
A Consultant Dermatologist or Consultant Paediatrician should confirm the diagnosis
Finding adult mites, eggs or faecal particles (scybala) may all confirm the diagnosis.
General measures
Latex gloves and plastic aprons must be worn when attending to the patient before and
during treatment. Scabies cannot be transmitted 24 hours after treatment with an effective
scabicide. Isolation is unnecessary for common scabies, but patients with crusted scabies
should be isolated until infection is clear.
Management of single case of ‘ordinary’ scabies (=index case)
Treat index case and some contacts.
A contact is defined as:
 All household (i.e. someone who lives in the same house) and ‘sexual’
contacts of the index case.
 The patient’s visitors during the in-patient stay (where there has been a
likelihood of prolonged (at least 10 minutes) skin-to-skin contact e.g. hand
holding).
 The patient’s carer (nurse, OT, etc) where there has been a likelihood of
prolonged (as above) skin-to-skin contact.
Staff will be advised to attend the Occupational Health Department; other contacts (e.g.
visitors, relatives) should be referred to their own GP promptly for treatment, even if they
have no symptoms.
Management of 2 or more linked cases of scabies (i.e. when an outbreak is
defined).
Treat all cases and contacts.
The Hospital Infection Control Doctor (HICD) working with the dermatologist and the
Consultant in Communicable Disease Control (CCDC), should decide which contacts (e.g.
patients, staff in hospital, household or other relevant persons) require prophylactic
treatment. This will amount to those suspected to have had prolonged (at least 10 minutes)
skin-to-skin contact with the cases in question. Failure to do so may lead to persistence of
infection.
Management of crusted scabies


Treat all known and suspected cases and contacts.
Index case(s) need to be treated.







Patients should be isolated until infection is clear. This may take days or even
weeks.
Gloves and long sleeved gowns should be worn when coming into close (skin-toskin) contact.
Staff and other contacts must be treated as described above.
CCDC should be informed if patient comes from nursing home or similar
institution.
Secondary contacts of staff and patient(s) should be advised to see their GP to
discuss treatment.
Contacts of confirmed secondary cases should be treated without delay.
Recently used underclothes, bed linen and towels should be machine washed at
temperatures above 50C, or kept in plastic bags for at least 72 hours to contain
mites until they die
Recommended Drugs Table
Drug
Available as
Permethrin
Lyclear
Cream
Malathion
(<2 yrs old)
Derbac-M
Strength/form
Dermal 5% cream
Quellada-M liquid
0.5% aqueous
liquid
0.5% liquid
emulsion
Application
Apply to whole body except head and face, wash off
8-12 hours later. Repeat once after 7 days if
necessary.
Apply to whole body except head and face, wash off
after 24 hours. Repeat after 7 days if necessary.
Vaccination and antimicrobial prophylaxis for patients undergoing elective or emergency
splenectomy or those who are asplenic or have a dysfunctional spleen
Overwhelming infection is a major risk in patients with an absent or dysfunctional spleen
and although uncommon, is associated with a high mortality. These infections are often due
to encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae type b
and Neisseria meningitidis and more than half of those infected die. Other serious infections
include malaria, babesiosis (caused by tick bite) and Capnocytophagia canimorsus (caused by
dog bites) and secondary infections following
Adults vaccination summary
Elective Splenectomy
Immunise at least TWO (ideally four to six) weeks prior to surgery.
Prophylactic antibiotics to start post surgery.
Emergency Splenectomy
Immunise ideally at least TWO weeks post surgery, or immediately before discharge from
hospital.
Prophylactic antibiotics to be started immediately.
Vaccine
Dosage/regimen
Re-immunisation
Pneumococcal vaccine
polyvalent
(Pneumovax II)
Pneumovax II, single dose of
(0.5mL im)
Hib and
Meninogococcal
Conjugate Group C
(Menitorix)
Previously unimmunised:
Two doses 0.5mL im of Hib/MenC
(menitorix) two months apart.
Previously fully immunised:
Offer reinforcing dose of 0.5mL im
of Hib/MenC (Menitorix)
Influenza
Adults should receive yearly
immunisation via their G.P.
(September to April)
Single dose 0.5mL deep sc of ACWY
Vax
Meningococcal ACWY
(ACWY Vax)
Only if travelling to
high risk areas (see
main guidance)
Adults and Children > 10
years:
Reimmunise every 5 years or
sooner if high risk patient
(sickle cell anaemia or
lymphoproliferative
disorders)
Not currently recommended
Yearly (September to April)
Reimmunise after 5 years if
still at high risk
Lifelong Adult antibiotic prophylaxis summary
Prophylaxis
Duration
First line
Penicillin V 500mg bd
If penicillin allergy
Erythromycin 500mg bd
Minimum 2 year
prophylactic course but
preferably lifelong



Indications for Percutaneous Coronary
Intervention (PCI)
Single or two vessel coronary disease
Previous CABG (sometimes - see below)
Triple vessel disease where CABG high risk
Indications for CABG




Symptomatic but unsuitable for PCI
Left main stem stenosis 50%
Proximal triple vessel disease
Two vessel disease including proximal
left anterior descending stenosis
Indications for referral to Cardiologist



Prognostic Assessment. The National Service Framework for Coronary
Heart Disease1 recommends that all patients thought to have new onset
angina should, unless thought unsuitable for revascularisation because of
frailty, intercurrent illness etc., be referred for prognostic assessment by
means of treadmill or other testing.
Diagnostic Uncertainty.

Refractory Symptoms despite full pharmacological treatment as outlined
below.

Suddenly Worsening or Unstable Symptoms may require urgent or
emergency referral.

Angina with a murmur needs investigating further (e.g. with
Echocardiography) to exclude haemodynamically significant valve disease.
4. Indications for Exercise Testing

Diagnostic - if the aetiology of chest pain (or dyspnoea) is in doubt
(except in the presence of Left Bundle Branch Block). Positive predictive
accuracy depends on the prevalence of the disease in the population
being tested (e.g. is very low in younger women with few risk factors and
atypical symptoms).

Prognostic - to identify those patients who may need revascularisation on
prognostic grounds. Exercise testing for this reason may not be necessary
in the elderly in whom symptom control is more important than long-term
prognosis.

Therapeutic - to reassure some patients that they can exercise safely
(e.g. post AMI).
Alternatives to Exercise Testing
Isotope perfusion (MIBI) scanning / Stress Echocardiography
These techniques may be used instead of ECG based stress testing, in the
presence of Left Bundle Branch Block or other pre-existing ECG abnormalities
(such as LVH) or where the ECG changes on exercise testing are equivocal
It is the investigations of choice in young/middle aged women with chest pain
if clinically indicated.
Exercise Testing in RBBB, especially if QRS duration is prolonged, may lead
to difficulties of interpretation.
Stress Echo is the recommended non-invasive test for reversible ischaemia in
end-stage CRF.
They can be used to determine whether a particular angiographically
demonstrated stenosis is causing reversible ischaemia.
Pharmacological stress (eg Dipyridamole, Dobutamine or Adenosine) may be
used in patients who are unable to exercise for non-cardiac reasons.
Treatment to relieve symptoms


-Blockers : All angina patients should be on a -blocker unless
contraindicated.
Impaired left ventricular function is an indication for, rather than a
contraindication to, -blockade. Bisoprolol and Carvedilol are
particularly indicated for patients with impaired left ventricular
function
Potassium Channel Openers
Nicorandil (10mg bd increasing after 2 weeks to 20mg bd) may be useful
in providing symptomatic relief.

Calcium Channel Blockers
Rate limiting calcium blockers (such as Diltiazem or Verapamil) may be used as an
alternative when -blockers are contraindicated (e.g. in the presence of asthma or severe
PVD) but should be used with caution in the presence of -blockade because of the
possibility of excessive bradycardia. Once daily preparations are preferred.
Dihydropyridine calcium antagonists (such as Amlodipine or Nifedipine) may be used in
addition to -blockers if symptom control is inadequate.
All calcium antagonists (especially Verapamil) are negatively inotropic and should be
used with caution where contractility is already impaired.
Short acting Nifedipine has been shown to increase mortality in CHD patients.

Nitrates
GTN sub-lingual tablets or spray are useful for immediate prophylaxis of angina and in
producing relief of symptoms.
Long acting nitrate tablets, transdermal patches or buccal preparations can provide
useful symptomatic relief but should be prescribed with at least a six hour nitrate-free
period every 24hrs.

Ivabradine (Procorolan)
This new selective sinus node inhibitor specifically slows the sinus rate and can be used
in stable angina where β blockers are contraindicated (other than because of sinus
bradycardia). (Dose 5mg bd increasing to 7.5mg bd if necessary)
7. Indications for Coronary Angiography
Elective:

Limiting stable angina despite optimal medical therapy where patients may benefit
symptomatically from coronary revascularisation.

Where clinical characteristics or non-invasive investigations suggest that the patient has
an adverse prognosis and may benefit prognostically from coronary revascularisation.

To define coronary anatomy prior to valve surgery.

Where non-invasive tests have been inconclusive or negative, but the patient continues
to have symptoms, which are troublesome, severe or result in recurrent admission to
hospital, in order to define a management strategy.
Emergency:
 In unstable angina (acute coronary syndromes without ST elevation) where ischaemic
chest pain continues despite optimal medical treatment or there is evidence of high risk
(from ECG, Troponins, CRP etc). See separate guidelines, serial number CA2008

For continuing ischaemic chest pain despite optimal medical treatment in the immediate
period following acute myocardial infarction.
8. Indications for Percutaneous Coronary Intervention
Limiting or unstable angina despite optimal medical treatment where the coronary anatomy
is considered suitable:

Single or two vessel coronary disease.

Previous CABG with native coronary anatomy suitable for PCI or with bypass graft
disease particularly when repeat CABG is regarded as an inappropriate revascularisation
strategy.

Triple vessel disease where the coronary anatomy is considered suitable for PCI
particularly when CABG is regarded as high risk because of poor left ventricular function
or disease co morbidity.
Indications for Coronary Artery Bypass Grafting
Symptomatic
Limiting or unstable angina despite optimal medical treatment where the coronary
anatomy is considered unsuitable for PCI (see above).
Prognostic



Left main stem stenosis of 50% or greater.
Proximal triple vessel disease.
Two vessel disease including significant proximal Left Anterior Descending stenosis –
particularly if left ventricular function is impaired
‘Thromboprophylaxis’.
Risk Factors
Previous DVT / PE
Cancer, particularly metastatic / pelvic
Hemiparetic stroke
Myocardial infarction
Thrombophilia
Varicose veins
Heart failure
COPD
Severe infection / dehydration
Inflammatory bowel disease
Rheumatic diseases
Polycythaemia
Nephrotic syndrome
Diabetic coma
Pregnancy / oestrogen therapy
Age > 70 years
Obesity (BMI >30)
Lower limb paralysis
Enoxaparin
 Consider thromboprophylaxis with Enoxaparin 40 mg od in any immobilised
medical patient with one or more of the above risk factors.
 Encourage mobilisation & ensure adequate hydration in all patients.
 Thromboprophylaxis may be inappropriate in patients who are terminally ill.
 Avoid Enoxaparin in stroke patients, unless very high risk for DVT / PE and cerebral
haemorrhage has been excluded (consultant decision). Use anti-embolism
stockings and aspirin (aspirin only if haemorrhagic stroke excluded) instead.
 In pregnancy use Tinzaparin 4500 IU once daily for prophylaxis in preference to
enoxaparin

Contraindications to prophylactic Enoxaparin include:
o Bleeding disorders, already receiving therapeutic anticoagulation, known
hypersensitivity to heparin, previous heparin induced thrombocytopaenia or
thrombosis, haemorrhagic stroke, active gastro-intestinal bleeding, acute MI
or acute coronary syndrome receiving high dose LMWH.

Caution in renal failure, reduce dose to Enoxaparin 20 mg od if eGFR < 30
mL/min/1.73m2).
If performing epidural or spinal anaesthesia, lumbar puncture or epidural catheter
removal, more than 12 hours should have lapsed since the last dose of enoxaparin.
Enoxaparin can be administered 4 hours AFTER the above procedures have been
performed (see Trust guideline CA2031).

Anti-embolism stockings
 Anti-embolism stockings should be considered for use as an alternative to
Enoxaparin where contra-indications exist, such as in acute stroke. They should be
properly fitted and worn until the patient is fully mobile or the risk of
thromboembolism is considered to be minimal.
 Contraindications to anti embolism stockings include:
 Dermatitis, ulceration, gangrene, peripheral vascular disease, leg deformity
preventing proper application, recent skin graft and severe leg oedema.
Varicella - Zoster Virus (VZV).
(VZV) is a herpes virus which causes 2 distinct clinical syndromes - chickenpox
and shingles.
Chickenpox.
Chickenpox is the primary infection and is predominantly an infection of
childhood. It may begin with a flu-like illness for 1-2 days before onset of the
rash. Skin lesions develop in crops and progress from macules through
papules and vesicles to scabs over several days. Virus can be isolated from
vesicle fluid and the base of fresh lesions.
The incubation period is 10 - 21 days, usually about 14 days, but may be
prolonged in immunocompromised patients. Infectivity commences for 1-2
days, but may be as long as 4 days before onset of rash, and persists until
crusts have formed, usually about 5 days after rash appears.
Shingles
Shingles is due to the reactivation of latent VZV. It can occur at any age but
most patients are over 50 years. The disease often begins with paraesthesiae
in the involved segment for 2-3 days. Erythematous maculopapular lesions
develop which rapidly evolve into vesicles and may coalesce to form bullae.
Infectivity persists for 5-7 days after onset of rash although immunocompromised patients may be infectious for longer.
Varicella (Chickenpox) is an acute, highly infectious disease caused by the Varicella
Zoster Virus (VZV). In hospitals Varicella infected persons have transmitted the
illness to susceptible persons through airborne routes and without having direct
contact.
Groups most at risk of serious illness if infected include:
*
*
*
*
*
*
patients with leukaemia and other haematological and nonhaematological malignancies.
transplant recipients
patients with AIDS
patients on high dose steroids
neonates
pregnant women.
The Department of Health PL CMO (2003)8: Chickenpox (Varicella) immunisation for
Health Care Workers (HCWs).recommended that Health Care Workers with a negative
or uncertain history of chicken pox should be serologically tested and vaccine offered
to those without Varicella zoster antibody
HCWs who develop a rash after having the vaccine should report to Occupational
Health before having patient contact.
Responsibility of Managers
To ensure all staff within their environments attend immunisation updates when
commencing employment within the trust.
To inform infection control and occupational health if a member of staff or
patient is diagnosed / exposed to VZV.
1. Immunocompromised patients with no/equivocal history of VZV infection and all
bone marrow transplant recipients.
i)
Take clotted blood for VZV serology. Include on request form whether
patient has been given VZIG or blood transfusion recently. Booking bloods
from pregnant women may be stored in the microbiology laboratory thus
negating the need for venepuncture
ii) Seek advice from the Duty Virologist in the microbiology department about
the use of VZIG (see later)
iii) Isolate the patient immediately until 21 days after last exposure. If the
patient is shown serologically to be immune, discontinue isolation.
iv) If the patient is susceptible take a second serum 2-3 weeks after exposure.
On the request form indicate if VZIG was given.
b. Immunocompromised patients with a positive history of VZV infection (with the
exception of bone marrow transplant recipients - see above) No further action.
a. Immunocompetent patients with no/equivocal history of VZV infection (who are
in a location where they may become a source of infection to
immunosuppressed individuals)
i)
Take clotted blood for VZV serology. Include on request form whether
patient has been given VZIG or blood transfusion recently.
ii) If the patient cannot be discharged, he/she must be isolated from 8 days
after first contact until 21 days after last contact. If VZV serology shows
immunity, isolation can be discontinued.
iii) If the patient is susceptible, take a second serum 2-3 weeks after exposure.
d. Immunocompetent patients with a positive history VZV infection
No further action.
II. STAFF - RELATED INVESTIGATION
1. A history of VZV infection or serological status must be sought from all exposed
staff if not already available.
2.
a.
Staff with a positive history of VZV infection or serological evidence of immunity
No further action.
b.
Staff with no/equivocal history of VZV infection and significant exposure
i)
Take clotted blood for VZV serology. Include on request form whether
individual has been given VZIG or blood transfusion recently.
ii)
Pending results, staff should go off duty from 8 days after first contact until
21 days after last contact or be redeployed in a non-sensitive area if possible.
iii) If they are found to be immune - no further action.
iv) A second serum should be taken from susceptible staff 2-3 weeks after
exposure.
v)
Pregnancy-
Staff without VZ antibodies will be offered VZ vaccination.
do
not
immunize,
but
give
immunoglobulin
The Role of the Consultant in Emergency Medicine "On Call"
To provide senior clinical leadership to the ED. This will consist of providing direct clinical
care to individual patients, the supervision and support of doctors in training in EM and
other specialties and a close working relationshipwith Departmental and Trust
management teams to ensure safe systems and processes are in place for all patients
attending with emergent and urgent conditions
It is also expected that the consultant should be kept informed of any significant
departmental events that may represent clinical risk to individual or multiple patients,
including excessive attendance numbers, unusual case mix or staffing issues.
Communications of this nature will normally be dealt with by telephone advice and
support.
The on-call EM consultant will also provide required clinical leadership in the event of
“Major Incident” activation.
When on-call, an EM consultant should not be recalled to hospital solely to deal with a
build up of less serious cases, because of excessive waiting times for first assessment or
because of potential breaches in the DH operational emergency access standard ("4
hour target").
Chest Drain insertion:
Clinical governance leads in local organisations should audit current practice and develop local policies
to ensure:
• Chest drains are only inserted by staff with relevant competencies and adequate supervision
• Ultrasound guidance is strongly advised when inserting a drain for fluid
• Clinical guidelines are followed and staff made aware of the risks, reflecting the questions above
• Identify a lead for training of all staff involved in chest drain insertion
• Written evidence of consent is obtained from patients before the procedure, wherever possible
• Local incident data relating to chest drains is reviewed and staff encouraged to report further incidents
Minimising risks of suprapubic catheter insertion (adults only)
Risks include injury to the intestine and haemorrhage due to perforation of vascular structures in the pelvis.
 Indications for intubation (CATS)
 Reduced LOC (GCS 8, AVPU P)
 Respiratory failure
 Worsening tachypnoea
 >40mls/kg fluid resus (likely pulm oed)
 Impending cardioresp collapse
Mental Capacity Act Underlying principles
1. A person must be assumed to have capacity unless it is established that they lack capacity.
2 A person is not to be treated as unable to make a decision unless all practicable steps to help
them to do so have been taken without success.
3 A person is not to be treated as unable to make a decision merely because he or she makes an
unwise decision.
4
5

An act done or decision on behalf of a person who lacks capacity must be done in their best
interests.
The decision should be less restrictive of the person’s rights and freedom of action.
Assessment of capacity involves ‘2 stage test’
 Do they have an impairment or disturbance that affects the way their mind or brain
works (either temporary or permanent)
 Does the impairment or disturbance mean that they cannot make a specific decision at
the time it needs to be made.........
Can they make a decision?
 They are provided with and understand the relevant information
 They are able to retain that information in their mind
 They can use that information to make a decision (“weigh it in the balance”)
 They believe the information given
 They can communicate that decision.
 Usual approach to assessment of capacity
NICE Guidance
If a person appears to be calm but refuses potentially life-saving treatment, or expresses the wish to die
by suicide, the assumption of capacity could be rebutted by evidence that the person does not truly
comprehend the consequences of his or her decision, that the person is acting under the undue influence
of another, that the person’s emotional distress associated with the stated reason for wishing to be dead
is impairing his or her judgement, or that the person’s behaviour shows that he or she is deeply
ambivalent about the decision (for example if the person initially sought help for the effects of the selfharm).
The fact that a person has a mental disorder is not sufficient to override the assumption of mental
capacity. However, a mentally capable person who suffers from a mental disorder could be detained
under the Mental Health Act if the relevant criteria under that Act are satisfied. The Court of Appeal has
held that the compulsory treatment for the mental disorder of a person who has been detained under
Section 2 or 3 of the Act can involve treatment for the consequences of the mental disorder and for the
symptoms of the disorder (B. v. Croydon Health Authority [1995] 1 All ER 683). In this case, one of the
judges ruled that ‘it would seem strange to me if a hospital could, without the patient’s consent, give
him treatment directed at alleviating a … disorder showing itself in suicidal tendencies, but not without
such consent be able to treat the consequences of a suicide attempt. In my judgment the term “medical
treatment for mental disorder” in s.63 includes such ancillary acts’ (ibid., pp. 686–7). Therefore,
although it is not a common occurrence, compulsory treatment can include medical and surgical
treatment for the physical effects of self-harm if the self-harm can be categorised as either the
consequence of or a symptom of the patient’s mental disorder. If, in a particular case, staff are in doubt
about the extent of treatment permissible under the Mental Health Act, they should consider seeking
legal advice and, when necessary, a court ruling.
Relevance of AD in OD – can’t really cover suicide!
What is needed for AD covering life threatening illness (written, signed, witnessed, specify life
threatening illness)
Can’t refuse basic comfort (note this means the offer of food and water. AD can refuse ANH as is medical
treatment)
Clinicians must be satisfied of validity
 Assessment of validity – capacity at time of AD?
 Any thing done since to suggest change of heart?
AD and MHA – can’t refuse MHA in advance
Admission of patients with syncope in ED:
ADMIT – Hx of CCF or Dysrhythmia
- Chest pain
- Evidence of CCF or VHD
- ECG with ischaemia/dysrhythmia/BBB/long QTc
CONSIDER
- >60 years
- Hx of IHD
- FHx of sudden death
- Younger patients with exertional syncope