Fluid resuscitation burns

Indication: >15% total body area burns in adults (>10% children)

The main aim of resuscitation is to prevent the burn deepening
Most fluid is lost 24h after injury
First 8-12h fluid shifts from intravascular to interstitial fluid compartments
Therefore circulatory volume can be compromised. However fluid resuscitation causes more fluid
into the interstitial compartment especially colloid (therefore avoided in first 8-24h)
Protein loss occurs

Fluid resuscitation formula
Parkland formula
(Crystalloid only e.g. Hartman's solution/Ringers' lactate)
Total fluid requirement in 24 hours =
4 ml x (total burn surface area (%)) x (body weight (kg))
50% given in first 8 hours
50% given in next 16 hours
Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to
achieve this)
Points to note:
Starting point of resuscitation is time of injury
Deduct fluids already given

After 24 hours

Colloid infusion is begun at a rate of 0.5 ml x(total burn surface area (%))x(body weight (kg))
Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x(burn
area)x(body weight)
Colloids used include albumin and FFP
Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to the
inflammatory cascade in burns
High tension electrical injuries and inhalation injuries require more fluid
Monitor: packed cell volume, plasma sodium, base excess, and lactate

All local anaesthetics have a chemical bond linking an amine to either an amide or an
ester. Most local anaesthetics are of the amino- amide types, these have a more favorable side
effect profile and are more stable in solution. Procaine and benzocaine have
amino - ester groups, these are metabolised by pseudocholinesterases.

Ventricular tachcardia

Ventricular tachycardia (VT)is broad-complex tachycardia originating from a ventricular ectopic focus. It
has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

There are two main types of VT:

monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by
prolongation of the QT interval. The causes of a long QT interval are listed below

Causes of a prolonged QT interval

Congenital
Jervell-Lange-Nielsen syndrome
(includes deafness and is due to
an abnormal potassium channel)
Romano-Ward syndrome (no
deafness)
Drugs
amiodarone, sotalol,
class 1a antiarrhythmic
drugs
tricyclic antidepressants,
fluoxetine
chloroquine
terfenadine*
erythromycin
Other
electrolyte: hypocalcaemia,
hypokalaemia,
hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
Valves of the heart
Mitral valve Aortic valve Pulmonary valve Tricuspid valve
2 cusps 3 cusps 3 cusps 3 cusps
First heart sound Second heart sound Second heart sound First heart sound
1 anterior cusp 1 anterior cusp 2 anterior cusps 2 anterior cusps
Attached to chordae tendinae No chordae No chordae Attached to chordae tendinae


Acute intermittent porphyria

Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in
porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic
accumulation of delta aminolaevulinic acid and porphobilinogen. It characteristically presents with
abdominal and neuropsychiatric symptoms in 20-40 year olds. AIP is more common in females (5:1)

Features

abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common

Diagnosis

classically urine turns deep red on standing
raised urinary porphobilinogen (elevated between attacks and to a greater extent during
acute attacks)
assay of red cells for porphobilinogen deaminase
raised serum levels of delta aminolaevulinic acid and porphobilinogen

Pagets disease

Paget's disease is a disease of increased but uncontrolled bone turnover and is characterised by
architecturally abnormal bones. It is thought to be primarily a disorder of osteoclasts, with excessive
osteoclastic resorption followed by increased osteoblastic activity causing areas of sclerosis and
deformity. Paget's disease is common (UK prevalence 5%) but symptomatic in only 1 in 20 patients

Predisposing factors

increasing age
male sex
northern latitude
family history

Clinical features

bone pain (e.g. pelvis, lumbar spine, femur)
classical, untreated features: bowing of tibia, bossing of skull
raised alkaline phosphatase (ALP) - calcium* and phosphate are typically normal
skull x-ray: thickened vault, osteoporosis circumscripta

Indications for treatment include bone pain, skull or long bone deformity, fracture, periarticular Paget's

bisphosphonate (either oral risedronate or IV zoledronate)
calcitonin is less commonly used now

Complications

deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure
naesthetic agents


The table below summarises some of the more commonly used IV induction agents
Agent Specific features
Propofol Rapid onset of anaesthesia
Pain on IV injection
Rapidly metabolised with little accumulation of metabolites
Proven anti emetic properties
Moderate myocardial depression
Widely used especially for maintaining sedation on ITU, total IV anaesthesia and for
daycase surgery
Sodium
thiopentone
Extremely rapid onset of action making it the agent of choice for rapid sequence of
induction
Marked myocardial depression may occur
Metabolites build up quickly
Unsuitable for maintenance infusion
Little analgesic effects
Ketamine May be used for induction of anaesthesia
Has moderate to strong analgesic properties
Produces little myocardial depression making it a suitable agent for anaesthesia in those
who are haemodynamically unstable
May induce state of dissociative anaesthesia resulting in nightmares
Etomidate Has favorable cardiac safety profile with very little haemodynamic instability
No analgesic properties
Unsuitable for maintaining sedation as prolonged (and even brief) use may result in
adrenal suppression
Post operative vomiting is common

ower limb- Muscular compartments

Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment
<muscle< b=""></muscle<> Nerve Action
Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor

Deep posterior compartment
Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot

Lumbar spinal stenosis

Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or
other similar degenerative changes.
Patients may present with a combination of back pain, neuropathic pain and symptoms mimicking
claudication. One of the main features that may help to differentiate it from true claudication in the history
is the positional element to the pain. Sitting is better than standing and patients may find it easier to walk
uphill rather than downhill. The neurogenic claudication type history makes lumbar spinal stenosis a likely
underlying diagnosis, the absence of such symptoms makes it far less likely.

Pathology
Degenerative disease is the commonest underlying cause. Degeneration is believed to begin in the
intervertebral disk where biochemical changes such as cell death and loss of proteoglycan and water
content lead to progressive disk bulging and collapse. This process leads to an increased stress transfer
to the posterior facet joints, which accelerates cartilaginous degeneration, hypertrophy, and osteophyte
formation; this is associated with thickening and distortion of the ligamentum flavum. The combination of
the ventral disk bulging, osteophyte formation at the dorsal facet, and ligamentum flavum hyptertrophy
combine to circumferentially narrow the spinal canal and the space available for the neural elements. The
compression of the nerve roots of the cauda equina leads to the characteristic clinical signs and
symptoms of lumbar spinal stenosis.

Diagnosis
MRI scanning is the best modality for demonstrating the canal narrowing. Historically a bicycle test was
used as true vascular claudicants could not complete the test.

Treatment
Laminectomy
Cardiac physiology


The heart has four chambers ejecting blood into both low pressure and high pressure systems.
The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the
left.
At rest diastole comprises 2/3 of the cardiac cycle.
The product of the frequency of heart rate and stroke volume combine to give the cardiac output
which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are on
the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral examination.

Electrical properties

Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is
capable of contraction.
In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium
and conveyed to the ventricles via the atrioventricular node.
The sino atrial node is also capable of spontaneous discharge and in the absence of background
vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate
found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is
lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at
which point an action potential is generated.
Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA
node will depolarise first. The cells have a refractory period during which they cannot be re-
stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states
this time period is overridden and inadequate ventricular filling may then occur, cardiac output
falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic
fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline
binds to 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation.

Cardiac cycle



Image sourced from Wikipedia



Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic
pressure is high.


Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic
volume 130-160ml.


Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction.
AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected.
Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).


Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular
pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and
elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the
aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml
(i.e. Volume ejected).


Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave
associated with closure of the aortic valve increases aortic pressure. The pressure dip before this
rise can be seen on arterial waveforms and is called the incisura. During systole the atrial
pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed
ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure
falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the
neck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid this
occurrence if veins are inadvertently cut, or during CVP line insertion.

Mechanical properties

Preload = end diastolic volume
Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.

It states that for hollow organs with a circular cross section, the total circumferential wall tension
depends upon the circumference of the wall, multiplied by the thickness of the wall and on the
wall tension.
The total luminal pressure depends upon the cross sectional area of the lumen and the
transmural pressure. Transmural pressure is the internal pressure minus external pressure and at
equilibrium the total pressure must counterbalance each other.
In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs
during the ejection phase is due to physical change in heart size. It also explains why a dilated
diseased heart will have impaired systolic function.

Starlings law

Increase in end diastolic volume will produce larger stroke volume.
This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke
volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant
patients who need to increase their cardiac output.

Baroreceptor reflexes

Baroreceptors located in aortic arch and carotid sinus.
Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal
nerve.
They are stimulated by arterial stretch.
Even at normal blood pressures they are tonically active.
Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node.
*Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke
volume.
*Decreased sympathetic discharge to venous system causing increased compliance.
*Decreased peripheral arterial vascular resistance

Atrial stretch receptors

Located in atria at junction between pulmonary veins and vena cava.
Stimulated by atrial stretch and are thus low pressure sensors.
Increased blood volume will cause increased parasympathetic activity.
Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:
the Bainbridge reflex.
Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal
blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by
juxtaglomerular apparatus-Increase in angiotensin II.
Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Organ Transplant

A number of different organ and tissue transplants are now available. In many cases an allograft is
performed, where an organ is transplanted from one individual to another. Allografts will elicit an immune
response and this is one of the main reasons for organ rejection.

Graft rejection occurs because allografts have allelic differences at genes that code
immunohistocompatability complex genes. The main antigens that give rise to rejection are:

ABO blood group
Human leucocyte antigens (HLA)
Minor histocompatability antigens

ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies to
other groups. Group O donors can give organs to any type of ABO recipient whereas group AB donor can
only donate to AB recipient.

HLA System
The four most important HLA alleles are:


HLA A
HLA B
HLA C
HLA DR

An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, four
each = 8 alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLA
mismatching. However, the greater the number of mismatches the worse the long term outcome will be. T
lymphocytes will recognise antigens bound to HLA molecules and then will then become activated. Clonal
expansion then occurs with a response directed against that antigen.

Types of organ rejection

Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO
incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates
and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.

Hyperacute
Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility and
HLA Class I incompatible transplants will all fare worse in long term.

Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of
transplanted organ are susceptible and it may occur in up to 50% cases.

Chronic
Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other
immunosensitising events all increase the risk. Vascular changes are most prominent with myointimal
proliferation leading to organ ischaemia. Organ specific changes are also seen such as loss of acinar
cells in pancreas transplants and rapidly progressive coronary artery disease in cardiac transplants.


Surgical overview-Renal transplantation
A brief overview of the steps involved in renal transplantation is given.
Patients with end stage renal failure who are dialysis dependent or likely to become so in the immediate
future are considered for transplant. Exclusion criteria include; active malignancy, old age (due to limited
organ availability). Patients are medically optimised.
Donor kidneys, these may be taken from live related donors and close family, members may have less
HLA mismatch than members of the general population. Laparoscopic donor nephrectomy further
minimises the operative morbidity for the donor. Other organs are typically taken from brain dead or dying
patients who have a cardiac arrest and in whom resuscitation is futile. The key event is to minimise the
warm ischaemic time in the donor phase.

The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron
immediately prior to implantation and factors such as accessory renal arteries and vessel length are
assessed and managed.

For first time recipients the operation is performed under general anaesthesia. A Rutherford-Morrison
incision is made on the preferred side. This provides excellent extraperitoneal access to the iliac vessels.
The external iliac artery and vein are dissected out and following systemic heparinisation are cross
clamped. The vein and artery are anastamosed to the iliacs and the clamps removed. The ureter is then
implanted into the bladder and a stent is usually placed to maintain patency. The wounds are then closed
and the patient recovered from surgery.

In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular necrosis
and this tends to resolve.

Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic twin
transplant (live donor) may survive as long as 25 years.
Voice production


There are 2 main nerves involved:

Superior laryngeal nerve (SLN)

Innervates the cricothyroid muscle

Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high notes during
singing, SLN paresis and paralysis result in:

a. Abnormalities in pitch
b. Inability to sing with smooth change to each higher note (glissando or pitch glide)

Recurrent laryngeal nerve (RLN)/Inferior laryngeal nerve

Innervates intrinsic larynx muscles

a. Opening vocal folds (as in breathing, coughing)
b. Closing vocal folds for vocal fold vibration during voice use
c. Closing vocal folds during swallowing

Hormonal regulation of calcium
Hormone Actions
Parathyroid hormone (PTH) Increase calcium levels and decrease phosphate levels
Increases bone resorption
Immediate action on osteoblasts to increase ca
2+
in
extracellular fluid
Osteoblasts produce a protein signaling molecule that activate
osteoclasts which cause bone resorption
Increases renal tubular reabsorption of calcium
Increases synthesis of 1,25(OH)2D (active form of vitamin D) in
the kidney which increases bowel absorption of Ca
2+

Decreases renal phosphate reabsorption
1,25-dihydroxycholecalciferol (the
active form of vitamin D)
Increases plasma calcium and plasma phosphate
Increases renal tubular reabsorption and gut absorption of
calcium
Increases osteoclastic activity
Increases renal phosphate reabsorption
Calcitonin Secreted by C cells of thyroid
Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

Dorsal column lesion Loss vibration and proprioception
Tabes dorsalis, SACD
Spinothalamic tract lesion Loss of pain, sensation and temperature
Central cord lesion Flaccid paralysis of the upper limbs
Osteomyelitis Normally progressive
Staph aureus in IVDU, normally cervical region affected
Fungal infections in immunocompromised
Thoracic region affected in TB
Infarction spinal cord Dorsal column signs (loss of proprioception and fine discrimination
Cord compression UMN signs
Malignancy
Haematoma
Fracture
Brown-sequard syndrome Hemisection of the spinal cord
Ipsilateral paralysis
Ipsilateral loss of proprioception and fine discrimination
Contralateral loss of pain and temperature

Coagulation cascade

Two pathways lead to fibrin formation

Intrinsic pathway (components already present in the blood)

Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK),
prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
Factor 12 activates Factor 11
Factor 11 activates Factor 9, which with its co-factor Factor 8a form the tenase complex which
activates Factor 10


Extrinsic pathway (needs tissue factor released by damaged tissue)

Tissue damage
Factor 7 binds to Tissue factor
This complex activates Factor 9
Activated Factor 9 works with Factor 8 to activate Factor 10

Common pathway

Activated Factor 10 causes the conversion of prothrombin to thrombin
Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form
links between fibrin molecules

Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption



Image sourced from Wikipedia


Intrinsic pathway Increased APTT Factors 8,9,11,12
Extrinsic pathway Increased PT Factor 7
Common pathway Increased APTT & PT Factors 2,5,10
Vitamin K dependent Factors 2,7,9,10


Upper limb fractures


Colles' fracture

Fall onto extended outstretched hands
Described as a dinner fork type deformity
Classical Colles' fractures have the following 3 features:

Features of the injury
1. Transverse fracture of the radius
2. 1 inch proximal to the radio-carpal joint
3. Dorsal displacement and angulation

Smith's fracture (reverse Colles' fracture)

Volar angulation of distal radius fragment (Garden spade deformity)
Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed

Bennett's fracture

Intra-articular fracture of the first carpometacarpal joint
Impact on flexed metacarpal, caused by fist fights
X-ray: triangular fragment at ulnar base of metacarpal

Monteggia's fracture

Dislocation of the proximal radioulnar joint in association with an ulna fracture
Fall on outstretched hand with forced pronation
Needs prompt diagnosis to avoid disability

Galeazzi fracture

Radial shaft fracture with associated dislocation of the distal radioulnar joint
Occur after a fall on the hand with a rotational force superimposed on it.
On examination, there is bruising, swelling and tenderness over the lower end of the forearm.
X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation
of the inferior radio-ulnar joint.

Barton's fracture

Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation
Fall onto extended and pronated wrist

Scaphoid fractures

Scaphoid fractures are the commonest carpal fractures.
Surface of scaphoid is covered by articular cartilage with small area available for blood vessels
(fracture risks blood supply)
Forms floor of anatomical snuffbox
Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal 1/3)
The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on
wrist movements and on longitudinal compression of the thumb.
Ulnar deviation AP needed for visualization of scaphoid
Immobilization of scaphoid fractures difficult

Radial head fracture

Fracture of the radial head is common in young adults.
It is usually caused by a fall on the outstretched hand.
On examination, there is marked local tenderness over the head of the radius, impaired
movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of
rotation (pronation and supination).

Benign liver lesions


Benign liver lesions
Haemangioma Most common benign tumours of mesenchymal origin
Incidence in autopsy series is 8%
Cavernous haemangiomas may be enormous
Clinically they are reddish purple hypervascular lesions
Lesions are normally separated from normal liver by ring of fibrous tissue
On ultrasound they are typically hyperechoic
Liver cell adenoma 90% develop in women in their third to fifth decade
Linked to use of oral contraceptive pill
Lesions are usually solitary
They are usually sharply demarcated from normal liver although they usually lack a
fibrous capsule
On ultrasound the appearances are of mixed echoity and heterogeneous texture. On
CT most lesions are hypodense when imaged prior to administration of IV contrast
agents
In patients with haemorrhage or symptoms removal of the adenoma may be required
Mesenchymal
hamartomas
Congential and benign, usually present in infants. May compress normal liver
Liver abscess Biliary sepsis is a major predisposing factor
Structures drained by the portal venous system form the second largest source
Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in
50%
Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in
chronic abscesses
Amoebic abscess Liver abscess is the most common extra intestinal manifestation of amoebiasis
Between 75 and 90% lesions occur in the right lobe
Presenting complaints typically include fever and right upper quadrant pain
Ultrasonography will usually show a fluid filled structure with poorly defined boundaries
Aspiration yield sterile odourless fluid which has an anchovy paste consistency
Treatment is with metronidazole
Hyatid cysts Seen in cases of Echinococcus infection
Typically an intense fibrotic reaction occurs around sites of infection
The cyst has no epithelial lining
Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick
and has an external laminated hilar membrane and an internal enucleated germinal
layer
Typically presents with malaise and right upper quadrant pain. Secondary bacterial
infection occurs in 10%.
Liver function tests are usually abnormal and eosinophilia is present in 33% cases
Ultrasound may show septa and hyatid sand or daughter cysts.
Percutaneous aspiration is contra indicated
Treatment is by sterilisation of the cyst with mebendazole and may be followed by
surgical resection. Hypertonic swabs are packed around the cysts during surgery
Polycystic liver
disease
Usually occurs in association with polycystic kidney disease
Autosomal dominant disorder
Symptoms may occur as a result of capsular stretch
Cystadenoma Rare lesions with malignant potential
Usually solitary multiloculated lesions
Liver function tests usually normal
Ultrasonography typically shows a large anechoic, fluid filled area with irregular
margins. Internal echos may result from septa
Surgical resection is indicated in all cases


Muscle relaxants

Suxamethonium Depolarising neuromuscular blocker
Inhibits action of acetylcholine at the neuromuscular junction
Degraded by plasma cholinesterase and acetylcholinesterase
Fastest onset and shortest duration of action of all muscle relaxants
Produces generalised muscular contraction prior to paralysis
Adverse effects include hyperkalaemia, malignant hyperthermia and lack of
acetylcholinesterase
Atracurium Non depolarising neuromuscular blocking drug
Duration of action usually 30-45 minutes
Generalised histamine release on administration may produce facial flushing,
tachycardia and hypotension
Not excreted by liver or kidney, broken down in tissues by hydrolysis
Reversed by neostigmine
Vecuronium Non depolarising neuromuscular blocking drug
Duration of action approximately 30 - 40 minutes
Degraded by liver and kidney and effects prolonged in organ dysfunction
Effects may be reversed by neostigmine
Pancuronium Non depolarising neuromuscular blocker
Onset of action approximately 2-3 minutes
Duration of action up to 2 hours
Effects may be partially reversed with drugs such as neostigmine


Image sourced from Wikipedia


Renal stones

Type of
stones
Features Percentage of all
calculi
Calcium
oxalate
Hypercalciuria is a major risk factor (various causes)
Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with calcium
making it more soluble
Stones are radio-opaque (though less than calcium phosphate stones)
Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
85%
Cystine Inherited recessive disorder of transmembrane cystine transport leading to
decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
1%
Uric acid Uric acid is a product of purine metabolism
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
5-10%
Radiolucent
Calcium
phosphate
May occur in renal tubular acidosis, high urinary pH increases supersaturation
of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2
and 4 do not)
Radio-opaque stones (composition similar to bone)
10%
Struvite Stones formed from magnesium, ammonium and phosphate
Occur as a result of urease producing bacteria (and are thus associated with
chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque
2-20%


Laxatives

Bulk forming laxatives
Bran
Psyllium
Methylcellulose
Osmotic laxatives
Magnesium sulphate
Magnesium citrate
Sodium phosphate
Sodium sulphate
Potassium sodium tatrate
Polyethylene glycol
Stimulant laxatives
Docusates
Bisacodyl
Sodium picosulphate
Senna
Ricinoleic acid


Diseases affecting the vertebral column


Ankylosing
spondylitis
Chronic inflammatory disorder affecting the axial skeleton
Sacro-ilitis is a usually visible in plain films
Up to 20% of those who are HLA B27 positive will develop the condition
Affected articulations develop bony or fibrous changes
Typical spinal features include loss of the lumbar lordosis and progressive kyphosis
of the cervico-thoracic spine
Scheuermann's
disease
Epiphysitis of the vertebral joints is the main pathological process
Predominantly affects adolescents
Symptoms include back pain and stiffness
X-ray changes include epiphyseal plate disturbance and anterior wedging
Clinical features include progressive kyphosis (at least 3 vertebrae must be involved)
Minor cases may be managed with physiotherapy and analgesia, more severe cases
may require bracing or surgical stabilisation
Scoliosis Consists of curvature of the spine in the coronal plane
Divisible into structural and non structural, the latter being commonest in adolescent
females who develop minor postural changes only. Postural scoliosis will typically
disappear on manoeuvres such as bending forwards
Structural scoliosis affects > 1 vertebral body and is divisible into idiopathic,
congential and neuromuscular in origin. It is not correctable by alterations in posture
Within structural scoliosis, idiopathic is the most common type
Severe, or progressive structural disease is often managed surgically with bilateral
rod stabilisation of the spine
Spina bifida Non fusion of the vertebral arches during embryonic development
Three categories; myelomeningocele, spina bifida occulta and meningocele
Myelomeningocele is the most severe type with associated neurological defects that
may persist in spite of anatomical closure of the defect
Up to 10% of the population may have spina bifida occulta, in this condition the skin
and tissues (but not not bones) may develop over the distal cord. The site may be
identifiable by a birth mark or hair patch
The incidence of the condition is reduced by use of folic acid supplements during
pregnancy
Spondylolysis Congenital or acquired deficiency of the pars interarticularis of the neural arch of a
particular vertebral body, usually affects L4/ L5
May be asymptomatic and affects up to 5% of the population
Spondylolysis is the commonest cause of spondylolisthesis in children
Asymptomatic cases do not require treatment
Spondylolisthesis This occurs when one vertebra is displaced relative to its immediate inferior vertebral
body
May occur as a result of stress fracture or spondylolysis
Traumatic cases may show the classic "Scotty Dog" appearance on plain films
Treatment depends upon the extent of deformity and associated neurological
symptoms, minor cases may be actively monitored. Individuals with radicular
symptoms or signs will usually require spinal decompression and stabilisation

Branches of the trigeminal nerve
Ophthalmic nerve Sensory only
Maxillary nerve Sensory only
Mandibular nerve Sensory and motor

Sensory
Ophthalmic Exits skull via the superior orbital fissure
Sensation of: scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose
(including the tip of the nose, except alae nasi), the nasal mucosa, the frontal sinuses, and parts of
the meninges (the dura and blood vessels).
Maxillary
nerve
Exit skull via the foramen rotundum
Sensation: lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal
mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses, and parts
of the meninges.
Mandibular
nerve
Exit skull via the foramen ovale
Sensation: lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw), parts
of the external ear, and parts of the meninges.

Motor
Distributed via the mandibular nerve.
The following muscles of mastication are innervated:

Masseter
Temporalis
Medial pterygoid
Lateral pterygoid

Other muscles innervated include:

Tensor veli palatini
Mylohyoid
Anterior belly of digastric
Tensor tympani
Neo-intimal hyperplasia in distal arterial anastamoses may be reduced by use of a Miller Cuff
when PTFE is the bypass conduit.

PTFE may induce neo-intimal hyperplasia with subsequent occlusion of the distal anastomosis. In more
proximal arterial bypass surgery the process of neo-intimal hyperplasia is not sufficient to cause
anastomotic occlusion. However, distal bypasses are at greater risk and if vein cannot be used as a
conduit then the distal end of the PTFE should anastomosed to a vein cuff to minimise the risk of neo-
intimal hyperplasia.
'Machine' - Causes of Increased Serum K
+


M - Medications - ACE inhibitors, NSAIDS
A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism, haemolysis
I - Intake - Excessive
N - Nephrons, renal failure
E - Excretion - Impaired

Familial periodic paralysis has subtypes associated with hyper and hypokalaemia.
Lower limb- Muscular compartments

Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe

Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint

Superficial posterior compartment
<muscle< b=""></muscle<> Nerve Action
Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor

Deep posterior compartment
Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot


Type of Murmur Conditions
Ejection systolic Aortic stenosis
Pulmonary stenosis, HOCM
ASD, Fallot's
Pan-systolic Mitral regurgitation
Tricuspid regurgitation
VSD
Late systolic Mitral valve prolapse
Coarctation of aorta
Early diastolic Aortic regurgitation
Graham-Steel murmur (pulmonary regurgitation)
Mid diastolic Mitral stenosis
Austin-Flint murmur (severe aortic regurgitation)

Causes of decreased compliance:
pulmonary oedema
pulmonary fibrosis
pneumonectomy
kyphosis
Causes of increased compliance
age
emphysema - this is due to loss alveolar walls and associated elastic tissue
A unilateral dilated pupil is a classic sign of transtentorial herniation.
The subclavian artery passes anterior to the middle scalene.