SAQs_



SAQs_

■ Elbow ossification centre- CRITOL

◆ Capitellum 6/12 - 2yrs

◆ Radial head 4yrs

◆ Internal (medial) epicondyle 6yrs

◆ Trochlea 8yrs

◆ Olecranon 10yrs

◆ Lateral epicondyle 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

◆ age15cm

◆ 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 (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 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) Factitious e.g. haemolysed sample.

ii) Reduced renal excretion – ARF, CRF, K+ sparing diuretics e.g. spironolactone.

iii) Cell injury e.g. burns, rhabdomyolysis.

iv) Hyperaldosteronism – Addison’s disease, drug induced (NSAID, ACE inhibitors).

v) K+ cellular shifts – acidosis from any cause (DKA), drugs (suxamethonium).

Clinical features include muscle weakness/ cramps, paraesthesiae, hypotonia.

Treatment

i) 10ml 10% calcium gluconate.

ii) 10u Actrapid with 50ml of 50% dextrose IV – helps cellular uptake of K+.

iii) Nebulised salbutamol.

iv) Careful fluid balance, correct acidosis with sodium bicarbonate.

v) ? calcium resonium.

vi) Correct underlying cause.

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 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) Cricopharyngeus

• ii) Aortic indentation

• iii) 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) Age ≥65 years

• ii) ≥3 CAD risk factors

• iii) Prior CAD (stenosis >50%)

• iv) Aspirin in last 7 days

• v) ≥2 anginal events in ≤24 hours

• vi) ST deviation

• vii) 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

[pic]

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 |

|[pic] |

|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 |

|1 - contains flexor digitorum profundus only distal to the insertion of 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 |

|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 |

|Flexor digitorum superficialis |

|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 |

|Sutures easily placed in the tendon |

|Secure suture knots |

|Smooth junction if the tendon ends |

|Minimal gapping at repair site |

|Minimal interference with tendon vascularity |

|Sufficient repair strength |

|Many techniques of tendon repair have been described |

|They invariably involve |

|Core suture |

|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 |

|Wrist at 0 - 30 degrees |

|MCP joints at 60 - 90 degrees |

|PIP and DIP joints in full extension |

|Hand should be elevated to reduce swelling |

|Early mobilisation required to |

|Reduce adhesion formation |

|Improve tendon healing |

|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). [ CLOSE WINDOW ]

[pic]

Neck trauma. Zones of the neck.

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. [ CLOSE WINDOW ][pic]Neck trauma. Zone I injury.

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. [ CLOSE WINDOW ]

[pic]

Neck trauma. Zone II injury.

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) Headache

ii) Fluctuating GCS

iii) Confusion

iv) Memory loss

v) 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

L lumbricals (lateral two)

O opponens pollicis

A abductor pollicis brevis

F flexor pollicis brevis

Look for:

• Index finger held in extension (Benediction attitude).

• Wasting of thenar muscles,

• deformity/ scars around wrist and elbow.

• Trophic changes.

Motor:

• 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 hypoxia

I infection

D drugs

D dural haemorrhage

E endocrine (hypoglycaemia)

N neoplasis / neurological

M metabolic (hypercalcaemia)

A alcohol (overdose, withdrawal, DT)

P psychosis

Causes for increased anion gap

M methanol

U uraemia

D DKA

P

I INH

L lactic acidosis

E ethylene glycol

A 45 year old man is referred to the ED by his GP. He had a two day history of progressive right-sided 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 Tetanus

Multiple sclerosis Spinal cord compression

Alcoholic myopathy Botulism

Poisoning (lead, organophosphates) 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 5.2 Bilirubin 74

WCC 3.9 ALT 25

Plt 195 AST 29

MCV 94 Alk phos 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

• Tachycardia, palpitations

• AF

• Cardiac failure

CNS

• Agitation, anxiety

• Tremor

• Delirium, coma

Other

• 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 4

Urinalysis NAD

What is the likely diagnosis?

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) Fluid resuscitation

ii) Check BM and treat if hypoglycaemic

iii) Take blood for cortisol and ACTH

iv) Hydrocortisone 100mg IV

v) 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.

[pic]

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) Malaise, low grade fever

ii) Hepatosplenomegaly

iii) Lymphadenopathy

iv) Colicky abdominal pain (may develop bloody diarrhoea, intussusception).

v) Arthritis/ arthralgia

vi) Testicular pain and/ or swelling

Causes of purpuric rashes in children:

i) meningococcaemia

ii) HSP

iii) thrombocytopenia 2° ITP, leukaemia, aplastic anaemia

iv) 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 fever, malaise, weight loss

Musculoskeletal athralgia, myalgia

Cutaneous butterfly rash, photosensitive rash, discoid lupus, Raynaud’s

Haematological thrombocytopenia, anaemia, leucopenia

Neuropsychiatric depression, psychosis, fits, CN lesions, ataxia

Renal glomerulonephritis, nephritic syndrome

CVS or RS pleurisy, pericarditis, pericardial/ pleural effusions

Apthous ulcers

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) Other infections e.g. herpes simplex, gonorrhoea.

ii) Neoplasms e.g. carcinoma of penis

iii) Behçet’s disease.

iv) 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. Age >55 yrs

2. WBC Count >16 x109/L

3. Blood Glucose >10 mmol/L (No Diabetic History)

4. Serum Urea >16 mmol/L ( No response to IV fluids)

5. Arterial Oxygen Saturation 7mmol/l.

• Respiratory rate: raised ≥30/min.

• Blood pressure: low BP systolic 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 3 days or major surgery within 4 weeks 1

4) localised tenderness along the deep veins 1

5) entire leg swollen 1

6) calf swelling 3cm more than asymptomatic side 1

7) pitting oedema confined to affected leg 1

8) dilated superficial veins 1

9) alternative diagnosis as likely or greater than DVT -2

Wells categorized patients into;

Low risk (score ≤0)

Moderate risk (score 1 or 2)

High risk (score ≥3)

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+ 350mmol/l (normal 280-305)

ii) no acidosis

ii) 6hrs old

iv) 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 D, T, P, polio, Hib, meningitis C

3 months D, T, P, polio, Hib, meningitis C

4 months D, T, P, polio, Hib, meningitis C

12-15 months MMR

3-5yrs D, T, P, polio, MMR

10-14yrs BCG

13-18yrs 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 dry mouth and a pulse rate of 150.

What is his maintenance fluid requirement?

Need to calculate percentage dehydration:

Mild (100 | 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 (250-500mg 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

• 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.

5.1 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 beta- lactam antibiotic

(this includes cephalosporins) or carbapenem, unless they have previously received a beta-lactam 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 12-24 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:

• 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:

• Fever

• Hypotension,

• 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 risk factor |2.5 |3/12 |

|proximal DVT or PE - idiopathic or permanent risk |2.5 |at least 6/12 |

|factor | | |

|VTE associated with Antiphospholipid syndrome |2.5 |while disease active |

| | |? lifelong |

|Recurrence of VTE while on Warfarin in therapeutic |3.5 |lifelong |

|range | | |

|Recurrence of VTE after cessation of warfarin |2.5 |review for permanent risk factors ? |

| | |lifelong |

|Cancer with VTE |2.5 consideration for therapeutic LMWH as|while cancer active |

| |an alternative | |

| |

|Cardiac Indications for valve replacements |

|Indication |Target INR |Minimum duration |

|Atrial Fibrillation |2.5 |Lifelong unless for cardioversion |

|Cardioversion |2.5 |Should be in therapeutic range (2-3) for |

| | |at least 4 wks before and 4 weeks after |

| | |cardioversion |

|Mural thrombus |2.5 |3/12 |

|Mechanical Mitral valve |3.0 |lifelong |

|Mechanical Aortic valve |2.5 |lifelong |

|Bioprosthetic (tissue) valve |None unless specified |None unless specified |

| |

|Other |

|Indication |Target INR |Minimum duration |

|Arterial thrombosis associated with |2.5 –3.5 |while disease active |

|anti-phospholipid syndrome | |? lifelong |

|Peripheral arterial thrombosis and grafts |antiplatelet drugs first line |long term |

| |if given – 2.5 | |

|Paroxysmal Nocturnal Haemoglobinuria |If clones >50% blood mononuclear cells |long term |

| |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. | |

Patient overanticoagulated

INR too high but 8 at 24 hours consider repeating dose of phytomenadione |

| |when INR 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 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, hepato-spleno 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 |DKA |HHS / HONK |

|Known to have diabetes? |Usually yes |Not as often |

|Duration of symptoms |Hours or days |Often days |

|Blood glucose (mmol/L) |>14 |>33 |

|Ketones in urine or blood? |Yes |Usually no |

|pH |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 =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 ................
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