Varicose Veins

Background

• Valve insufficiency in the veins (usually in the leg) cause a back up of pressure in the venous system.  Thin walled superficial veins are unable to cope with higher pressures and so dilate and become tortuous.
  • The most common valves involved are located at the sapheno-femoral junction
• Varicose veins are extremely common, with an incidence of around 2.5% of women and 2% of men.
  • Age, pregnancy, liver disease, previous DVT and family history all seem to increase the risk of varicose veins

History

• Quite often patients present without any symptoms – veins are bothering them because of aesthetic reasons
  • Important to ask about symptoms e.g. itching, discomfort, heaviness of the legs, night cramps, oedema, burning, paraesthesia, excercise intolerance, weakness, restless legs etc.
    • Classic picture is of dull ache which is worse with prolonged standing
  • Check SOCRATES i.e. onset, duration, timing/change, exacerbating/alleviating factors etc
• Make sure also to ask about
  • PMHx- Varicose veins (and any previous assessments/management), DVT, trauma, oedema, liver problems, cardiovascular disease; and Drug history
  • Social history- in particular, occupation that may involve prolong standing

Examination

• Inspection
  • Inspect both legs fully exposed with the patient standing first
    • Usually inspect from the anteromedial aspect of the thigh to the lateral aspect of the leg (long saphenous vein route); and then the back of the calf (short saphenous)
    • Look also for skin changes e.g. haemosiderin deposition, eczema, ulcers, thinned skin etc
• Palpation
  • Palpate the varicosities for tenderness (thrombophlebitis- normally should be painless); if they are hard this may suggest thrombosis
    • See if the veins will empty and refill with palpation
  • Palpate the skin if there any changes
  • Cough impulse test (whilst standing- tests for saphenofemoral insufficiency)
    • Locate the saphenofemoral junction by locating the femoral pulse then moving medially (vein) then two fingerbreadths inferiorly
    • Compress the area and ask the patient to cough
      • If a ‘thrill’ is felt, suggests that the valve here is incompetent
  • Elevate the leg to around 15 degrees and check the rate of vein emptying
• NB Other special tests e.g.
  • Trendelenberg test (tests for the location of the incompetent valve using a tourniquet at the level of the saphenofemoral junction to prevent refilling on standing- shows incompetence at the level of the SFJ; Note the tourniquet can be applied lower down the leg to check at which level the incompetence arises)
  • Perthes’ manoeuvre (using a tourniquet to prevent superficial filling and asking the patient to activate calf muscles by standing on tip toes repeatedly- normally emptying the varicosities by paradoxically filling in deep vein obstruction) have been used in the past but have now become surplus due to evaluation by Doppler USS.
• You should also auscultate varicosities and check for pitting oedema and peripheral pulses (a JVP assessment may also be appropriate where oedema is present).

Management

• Lifestyle – although unlikely to reverse the process, losing weight and exercise will prevent deterioration and further varicosities
  • NB Compression stocking may also prevent further varicosities but are not recommended for management unless further management (intervention) is not possible)
• Interventional management
  • Endothermal ablation
  • USS guided foam sclerotherapy
  • Avulsion
  • Ambulatory phlebectomy
  • Injection sclerotherapy

Inpatient VTE prophylaxis

Venous thromboembolism (VTE) still accounts for a significant proportion of avoidable hospital deaths. In an effort to tackle this problem NICE produced guidelines in 2010.

Before admission

• advise women to consider stopping oestrogen-containing oral contraception or HRT 4 weeks before surgery.
• assess the risks and benefits of stopping antiplatelet therapy 1 week before surgery.

The following patients are deemed at risk of VTE

Medical patients

• if mobility significantly reduced for >= 3 days or
• if expected to have ongoing reduced mobility relative to normal state plus any VTE risk factor (see below)

Surgical patients and patients with trauma

• if total anaesthetic + surgical time > 90 minutes or
• if surgery involves pelvis or lower limb and total anaesthetic + surgical time > 60 minutes or
• if acute surgical admission with inflammatory or intra-abdominal condition or
• if expected to have significant reduction in mobility or
• if any VTE risk factor present (see below)

VTE risk factors

• active cancer or cancer treatment
• age > 60 years
• critical care admission
• dehydration
• known thrombophilias
• obesity (BMI > 30 kg/m²)
• one or more significant medical comorbidities (for example: heart disease; metabolic, endocrine or respiratory pathologies; acute infectious diseases; inflammatory conditions)
• personal history or first-degree relative with a history of VTE
• use of HRT
• use of oestrogen-containing contraceptive therapy
• varicose veins with phlebitis

In-patient VTE prophylaxis

As a general rule pharmacological VTE prophylaxis is used for medical patients unless there is a contraindication.

For surgical patients mechanical VTE prophylaxis is offered for patients at risk. Pharmacological VTE prophylaxis is also given for if the risk of major bleeding is low.

Pharmacological VTE prophylaxis options:

• fondaparinux sodium
• low molecular weight heparin (LMWH)
• unfractionated heparin (UFH) (for patients with renal failure)

Mechanical VTE prophylaxis options:

• anti-embolism stockings (thigh or knee length)
• foot impulse devices
• intermittent pneumatic compression devices (thigh or knee length)

Post-procedure VTE prophylaxis

For certain procedures pharmacological VTE prophylaxis is recommended for all patients, using one of the following:

• dabigatran, started 14 hours after surgery
• fondaparinux, started 6 hours after surgery
• LMWH, started 6-12 hours after surgery
• rivaroxaban, started 6-10 hours after surgery.

Central venous lines and Central venous pressure

Background

• Central venous cannulation is a relatively common procedure (particularly in anaesthesia/intensive care).
  • NB It is unlikely you will be asked to insert a central venous line as a junior doctor (let alone a student).  However, you may be asked to measure CVP from a central line or assist/observe one being inserted.

Indications

• Measurement of CVP and/or replacement of circulating volume (e.g. in patients in shock with failed fluid resuscitation)
• Infusion of irritant drugs and total parenteral nutrition
• Difficult peripheral access (last resort)
• Insertion of pacing wires or pulmonary artery catheters
• Haemofiltration/haemodialysis
• Long-term IV treatments e.g. chemotherapy or antibiotics

A note about catheters

• There are many different types and sizes of catheters used in different situations
  • In general- wide bore cannulae are used in resuscitation and haemofiltration (BUT increased risk of haemorrhage and air embolus during insertion and thrombosis and subsequent stenosis); whilst narrow lumen cannulae are better suited for administering vasoactive drugs
• There are also several different sites for CVC insertion including the internal jugular vein, the subclavian vein, the femoral vein, the external jugular vein and peripheral veins (commonly the Basilic or Cephalic veins in the antecubital fossa)
  • Whilst sites vary depending on the patient and indication, in general,
    • internal jugular vein is favoured for acute vasoactive drug administration and regular CVP monitoring
    • the subclavian is favoured for resuscitation and CVP monitoring
    • the peripheral veins are favoured for prolonged therapies

Insertion

• Central venous catheters are generally inserted using the Seldinger technique
  • 
• For instructions on how to insert CVCs, see here (FRCA website).
  • NB ALWAYS use aseptic technique
• ALWAYS carry out a CXR after CVC insertion to check position.

Potential Complications

• Haemorrhage- particularly those on warfarin/other anticoagulation or with clotting disorders
• Occlusion- either from thrombosis or a kinked tube.  The CVC requires regular flushing to avoid haemostasis and a secure dressing to prevent tube problems.
• Infection- redness, pain and inflammation around the site may indicate infection.  Aseptic techniques should be used when inserting catheters and clean techniques used when measuring/removing/using etc.
• Air embolus- if a line becomes disconnected there is a risk of air embolus.  Lines should be checked regularly to avoid this.
• Catheter displacement- occasionally catheters can fall into the right atrium and ventricle and cause arrhtyhmias which should be noted and managed ASAP.

Measuring CVP

• Manually using a manometer
  • WIPE (wash hands, introduce self, check patient details, explain and gain consent)
  • If IV fluid is not running, ensure the CVC is patent by flushing the catheter with normal saline
  • Place the patient flat in the supine position (if possible)
  • Line up the manometer arm with the phlebostatic axis (this is the intersection between the 4th IC space and the mid-axillary line- almost at the level of the right atrium), and ensure the bubble is between the two lines of the spirit level.
  • Move the manometer scale up and down to allow the bubble to be aligned with 0 on the scale (zeroing the manometer)
  • Turn the three way tap off to the patient and open to the manometer
  • Open the IV fluids and slowly fill the manometer to a level higher than the expected CVP
    • NB Normal CVP is 3-8 cm H20 (some say 5-10cmH20) or 2-6 mmHg
  • Turn the 3-way tap on to the patient- the fluid level should fall until gravity equals the pressure.
    • If the pressure varies with patient breathing, take the lowest value.
  • Turn the tap off to the manometer.
  • Record CVP, wash hands and thank the patient,
• Using the transducer
  • WIPE
  • The CVC will be connected to fluids under pressure- ensure that the pressure is up to 300mmHg.
  • Place the patient flat in the supine position (if possible)
  • Often there will be multiple transducer ports to choose from (commonly the white port is used for CVP measurement- BUT CHECK)
  • Tape/secure the port to the phlebostatic axis or as close as possible to the right atrium.
  • Turn the tap off to the patient and open to the air by removing the cap from the three way port.
  • Press 0 on the monitor to zero the transducer.
  • Replace the cap and turn the tap on to the patient.
  • Observe the CVP trace and level- record the CVP.

Interpretation

• NB Interpret in conjunction with presentation and other investigations
• Raised CVP
  • Increased intrathoracic pressure
  • Impaired cardiac function (only useful for right heart evaluation)
  • Hypervolaemia
  • SVC obstruction
• Decreased CVP
  • Hypovolaemia
  • Reduced IT pressure (e.g. inspiration)

Pulmonary Function Tests

Background

• These can be useful in evaluating the nature and severity of respiratory disease BUT must always be interpreted in context of the patient history and examination

Indications

• To evaluate presentations of lung disease (most commonly dyspnoea and hypoxia, but also for others e.g. hypercapnia, cyanosis, wheezing etc)
• To assess progression of lung disease (NB more commonly this is done using peak flow monitoring but PFTs can also be a more formal measure, particularly if you suspect more than one underlying cause)
• To evaluate patients pre-operatively

Components

• Spirometry
  • Measures the air movement in and out of the lungs during respiratory maneouvres e.g. forced inspiration and expiration
    • It can measure volumes and speeds of air movement (i.e. FEV1)
    • Most useful at measuring the FVC, FEV1 and FEV1/FVC ratio

 

• Spirometry can also be used to produce a flow-volume loop (showing the same thing but volume is plotted on the x-axis and flow is plotted on the y-axis.  These can be useful in estimating the kind of obstruction.

Note that volume is plotted backwards on this volume loop

 

• Diffusing capacity
  • A further PFT which uses labelled Carbon monoxide to measure the ability of the lungs to diffuse and transfer gases- which can subsequently be used as a measure of functional lung surface area and thus total lung volume.
  • It is most commonly used to evaluate restrictive pattern diseases or spirometry results that have not been responsive to bronchodilators.
  • Common causes of reduced capacity include
    • **Anaemia (remember non-respiratory causes- take into context)
    • Emphysema, ILD, Po Oedema, Po vascular disease

Interpretation

1. Is the FEV1/FVC ratio less than the lower limit of normal (0.70 is the normal cut off for obstructive disease; >0.75 is regarded normal)?
   1. Obstructive or not?
2. Is the FVC less than the lower limit of normal? (NB Normal FVC is calculated based on age, size/weight/height etc)
   1. Any restrictive component or not?
3. Is the total lung capacity known?
   1. Reduced in true restriction and normal in pseudo-restriction

Examination of the Thyroid Gland

• WIPE
  • Wash hands, introduce self, check patient details, explain role and gain consent
• General Inspection
  • Is the patient obviously over-/under-weight?
  • Are they agitated/restless?
  • Are they wearing appropriate clothes for the weather/temperature (e.g. too many layers indoors)?
  • Do they look sweaty?  (If you shake their hand, is it sweaty?)
  • Does their voice sound normal?
• Hands
  • Inspect the hands for any erythema, look at the fingers for any thyroid acropachy (similar to clubbing), and feel for sweating/dryness and temperature.
  • Ask the patient to hold hands out in front of them to look for postural tremor
    • If this is not clearly evident, it may be helpful to place a sheet of paper over the hands to more closely observe any tremor.
• Pulse
  • Assess rate, rhythm (wary of AF), volume/strength, etc
• Face
  • Look for any sweating/dryness;
  • look at the eyes- are they ‘puffy’, are they obviously protruding
    • Further inspect the eyes from the side and from above to assess for exomphalos/proptosis
    • Look for any lid retraction
    • Also assess eye movements
      • On downward movements- assess any lid lag
      • Ask about any double vision
      • Assess pupils (occasionally Graves’ disease can also produce a RAPD)

NB You may want to examine the thyroid/neck now or at the end (depending on time and/or extent of examination)- see other things to examine at the end of this post.

Examination of the thyroid

• Inspection
  • Ensure adequate exposure of the neck (my require undoing several top buttons)
  • Inspect from the front and sides for any visible scars/goitre/asymmetry
    • Ask the patient to swallow some water and further inspect the movement in the neck
      • If a swelling moves, it is likely to be associated with the thyroid
    • Ask the patient to stick out their tongue (if mass moves- potentially a thyroglossal cyst)
• Palpation
  • Place the middle 3 fingers of each hand along the midline of the neck, locate the upper edge of the thyroid cartilage (Adam’s apple) and move inferiorly until you reach the cricoid cartilage/ring- the thyroid isthmus overlies this area and the lobes lateral and slightly inferior to this
  • Palpate using the pads of your fingers (not tips)
    • Ask the patient to swallow some water whilst you palpate the thyroid- you should feel symmetrical elevation of the thyroid lobes
    • Also ask the patient to stick out their tongue
  • Assess
    • Size; symmetry; consistency; masses; palpable thrill
  • It is a good idea to also examine the lymph nodes; you may also want to palpate the trachea to check for any deviation
• Percussion
  • Percuss from the sternum down (retrosternal dullness could indicate a large thyroid mass)
• Auscultation
  • Auscultate the thyroid lobes for vascular bruits

Further tests (if appropriate- NB mention in an OSCE, you may or may not be asked to do these)

• Test reflexes (hyporeflexia may be seen in hypothyroidism)
• Inspect the shins for pre-tibial myxoedema (Graves’)
• Assess for proximal myopathy by asking the patient to stand from sitting without using their arms (cross their arms)

Finish by thanking patient, washing hands and summarising findings

Further investigations usually involve FBC, U&Es, TFTs +/- scans (depending on findings)

Hypoglycaemia

Background

• Hypoglycaemia is generally defined as a blood glucose <4mmol/l (in DM- < 3mmol/l in non-diagnosed patients).  It should be treated as an emergency (i.e. managed as soon as identified)
• Most commonly occurs in patients with diabetes mellitus (usually those on insulin)
  • It is estimated that people with type 1 diabetes (i.e. insulin dependent) may have up to two episodes of mild hypoglycaemia a week
  • Note that the number of patients with DM in the hospital setting can make up to 25% of hospital patients
• Potentially serious and should be avoided

Risk factors

• Medical causes
  • Those related to diabetes:
    • Tight glycaemic control; PMHx of severe hypoglycaemia; Undetected nocturnal hypoglycaemia; Long duration of diabetes; Poor injection technique; impaired awareness of hypoglycaemia
    • Incorrect insulin dosages (commonly inappropriate stat/PRN doses; or inappropriately timed insulin doses at mealtimes)
    • Changing to sliding scale insulin or other form of insulin e.g. from basal to mixed
  • Other
    • Severe hepatic dysfunction
    • Renal dialysis/impaired renal function
    • Stopping steroids
    • Recovery after acute illness
    • GI upset (causing reduced calorific intake e.g. gastroenteritis, coeliac)
• Lifestyle
  • Increased exercise (relative to normal)
  • Irregular lifestyle
  • Age
  • Alcohol
  • Inadequate BM monitoring
  • Reduced carbohydrate intake

Clinical features

• Autonomic
  • Sweating
  • Palpitations
  • Hunger
  • Shaking
• Neuroglycopenic
  • Confusion
  • Drowsiness
  • Odd behaviour
  • Speech difficulty
  • Incoordination
• General
  • Malaise
  • Headache
  • Nausea

NB If a patient presents with several of these symptoms (particularly if they are diabetic), a bedside glucose and lab glucose should be taken.  It is also a good idea to review patients recent BMs and diabetes medications (including insulin) doses.

Grading Hypoglycaemia

• Mild
  • Patient conscious, orientated and able to swallow
• Moderate
  • Patient conscious and able to swallow but confused, disorientated or aggressive
• Severe
  • Patient is unconscious/fitting (or is very aggressive or nil by mouth)

Management

• Mild
  • Give 15-20g of quick acting carbohydrate e.g. 5-7 Dextrosol tablets, 4-5 Glucotabs, 90-120mls lucozade or 150-200mls pure fruit juice
  • Test BM/Glucose 15 minutes later
    • If still hypoglycaemic, repeat up to three times
      • If still hypoglycaemic, call for advice and consider IV 10% dextrose at 100ml/hour (or 1mg glucagon IM)
    • Follow up with 20g of longer-acting carbohydrate e.g. 2 biscuits, slice of bread etc
• Moderate
  • If capable, treat as mild hypoglycaemia.  If not but able to swallow, give 1.5-2 tubes of glucogel
    • If this is ineffective, give 1mg IM Glucagon
  • Re-check and repeat up to 3 times as with mild hypoglycaemia; seek advice if still hypoglycaemic following this
• Severe
  • Manage patient with ABCDE approach and seek help early
  • Once the patient is stable and hypoglycaemia confirmed with BM:
    • Give IV glucose stat (over 10 minutes)
      • either 75ml of 20% or 150ml of 10% dextrose (50% is NOT recommended)
      • +/- 1mg IM glucagon
    • Recheck glucose after 10 minutes- if still hypoglycaemic, repeat treatment
  • NB If hypoglycaemic due to NBM
    • once the patient has BM >4mmol/l- give 10% dextrose at 100ml/hr until no longer NBM (or reviewed by consultant and decision made to stop)
• In all patients, be sure to review daily BMs following hypoglycaemia

Examination of the Newborn

The newborn examination is carried out within 48 hours of birth, then again at 8 weeks (usually by the GP).

• WIPE
  • Wash hands, introduce self (ideally mother should be present), check mother and baby details* and explain the examination/gain consent
    • * Check name, DOB, gestational age, birth weight (and centile), delivery type, feeding (and how will they feed)/urinating/bowel movements (any meconium passed?- black, sticky stool), any parental concerns (ask specifically about family problems with hips, congenital heart problems etc)
      • NB this can be done whilst washing your hands or whilst parent/you are undressing the baby
• General inspection (Completely undress the baby down to nappy)
  • Note skin colour (any jaundice; any marks from birth, any obvious birthmarks); activity, posture, response
    • NB You will have to examine the baby’s back so best to leave general inspection of that until then- you may do this first or last.
• Head
  • Measure and record head circumference
  • Palpate the fontanelles and sutures
    • Note any tense fontanelles (remember this may be normal when the baby is crying but is relatively rare at rest)
    • NB It may be easier to do this whilst examining the baby’s back
  • Assess facial appearance- eye position and ear position; any asymmetry
• Eyes
  • If the baby has its eyes open, check the red reflex with an ophthalmoscope (congenital cataracts)
  • Look for any obvious signs of infection
• Ears
  • Note size, shape, symmetry and whether they are set normal or low
  • Check the patency of the external auditory meatus
    • Note that formal hearing testing is offered later
• Mouth
  • If possible, look into the mouth to look at the palate (any cleft?)
    • DO NOT use a tongue depressor; only use your finger (clean) and be gentle
  • With a clean finger, check the suckling reflex
• Limbs
  • Feel the baby’s bones, checking symmetry
  • Count fingers and toes (looking for any abnormalities); check palmar creases; look for talipes (club foot)
  • Check the baby’s tone (this does not have to be a rigid examination of tone)
  • Check the clavicles (may be disturbed during birth and cause Erb’s palsy)
  • Check the hips using Ortolani and Barlow’s tests to check for any developmental dysplasia
  • Check if there is a grasp reflex in both hands
• Chest
  • Look at the baby’s chest; check respiratory rate (normally 30-60bpm)
  • Listen to the heart sounds (normally 120-150bpm).  It can be difficult to hear any murmurs but you should try.
  • Also check the radial, brachial and femoral pulses (and any radio-femoral delay)
• Abdomen
  • Palpate the abdomen and inspect the umbilical stump for any signs of infection
• Groin/Genitals
  • Remove the baby’s nappy and inspect the genitals.  In male babies, check for both testicles (any undescended)
• Back and Anus
  • With the baby on their front, inspect the back, particularly at the neck and the sacrum (look for any dimples)
  • Feel down the spine, checking for any curvature
  • Check the patency of the anus
  • As you are turning the baby back, it is good point to check the Moro reflex
    • With you holding/supporting the baby’s back (so the baby is lying on your arm face up); suddenly lower the baby and stop suddenly
      • the moro reflex is abduction and adduction of the arms, usually accompanied by crying (primitive startle reflex)

Remember also to carry out screening tests e.g. heel prick at 5-8 days; sweat test; formal hearing test etc.

Psychiatric History

NB Before starting- consider (where possible) the patient’s details, the location of the consultation, the legal status of the patient, the reason for the consultation and who is the main source of the history (the latter is particularly important).

• WIPE (Wash hands, introduce self, check patient details and explain the nature of the consultation/develop some rapport)
• Presenting complaint(s)- find out what are the main concerns for the patient
• History of presenting complaint
  • When did you last feel well?
  • SOCRATES- i.e. when/how did things start; any triggers/exacerbating/alleviating factors etc; progression
    • NB a detailed analysis of each symptom e.g. low mood, should be done prior to discussing other symptoms
      • Onset/development/major events
      • Severity/frequency/persistance (e.g. good days/bad days)
      • Exacerbating/relieving factors
      • Impact on daily life
  • Ask about associated symptoms (if the patient has not mentioned them) after this (i.e. psychiatric systemic enquiry)
    • Sleep, diet, concentration/employment, weight, appetite, bowel habit, energy etc
• Present social situation
  • Where do they live? Who with? Support? Relationships? Social/family circle? Working? Alcohol/Drugs? Legal problems?
• Past Psychiatric history
  • Previous Dx and Mx- what has been tried and what has been effective
  • Any important similarities with this episode
  • Important to ask about suicide attempts if appropriate
• PMHx/Developmental Hx
  • Particularly any problems or major events (physical or emotional) in the past
  • Note ‘organic’ events e.g. meningitis; head injury; epilepsy etc
• Current and past RHx
  • And do they feel it works?
• FHx
  • Particularly of similar psychiatric conditions
• Past Social History/Personal History/Developmental History
  • Childhood- siblings, school, parents, events, learning
  • Education/jobs- able to cope reading/writing/numbers; past employment and duration at each; relationship with employer/colleagues
  • Activities (particularly if unemployed)- how do they fill time; anything they enjoy? How does the patient cope with stress?
  • Relationships/support, any children/family
  • Past Forensic history
  • Alcohol and drugs – CAGE
  • How would you describe your normal self (personality)?

Note that a history may be difficult in psychotic patients and that, throughout the consultation, you should be examining the patient’s mental state.  Different presenting complaints require a different approach (see Psychiatry Core Clinical Problems).

Interpretation of U&Es

Interpretation of U&Es can be broken into its two components i.e. Urea (Kidney function) and Electrolytes.  Note that the two should be interpreted in context of each other and the clinical scenario- many abnormalities seen in U&Es are not pathological (e.g. due to drugs, dehydration etc).

Renal Component (Urea and Creatinine)

• Physiology
  • Creatinine is produced in the liver (energy store for fast twitch muscle fibres)- it can be phosphorylated to store phosphate to produce ATP, after which it is excreted by the kidneys
    • Amount in blood depends on kidney function, liver function (much less so) and muscle mass (this latter component can be very important when interpreting creatinine levels)
  • Urea is produced from the breakdown of amino acids in the liver and is excreted by the kidneys too.
    • Whilst urea levels can be an indication for kidney function, there are many other things that may affect urea levels e.g.
      • Increase: dehydration; GI bleed; increased protein breakdown (post-op; trauma; infection; malignancy); drugs; high protein diet
      • Decrease: malnutrition; liver disease; pregnancy
• Normal values
  • Creatinine levels: typically 60-120μmol/l for men and 55-100μmol/l for women (NB labs will differ between reference ranges)
    • NB Creatinine can correlate with lean body mass (i.e. a cachexic old lady will have a significantly lower creatinine than a body builder but may still have an acute kidney injury)
      • it is important, where possible, to measure/estimate a baseline creatinine for the individual patient
  • Urea: around 2.5-8mmol/l
• Interpretation
  • A rise in both urea and creatinine suggests renal dysfunction
    • A rise in creatinine >50% above baseline is indicative of AKI
    • Other tests should be carried out to further evaluate kidney function e.g. urinalysis, FBC, blood gases (if patient is unwell), other electrolytes e.g. PO4 and Ca2+; CK; Immunoglobulins/complement; urine output etc
  • A solitary rise in urea (as suggested above) may not be due to kidney function- important to check fluid status

Electrolyte Component

• Sodium (135-145mEq/l or mmol/l)
  • Hyponatraemia
  • Hypernatraemia
    • Causes
      • In normovolaemic patients- commonly iatrogenic (e.g. excess IV saline or sodium containing drugs)
      • In dehydrated/hypovolaemic patients
        • can be due to sodium loss e.g. diarrhoea/vomiting, burns
        • or due to lack of reabsorption e.g. diabetes insipidus or osmotic diuresis (e.g. in DKA or hypoaldosteronism)
    • Investigations
      • Check serum and urine osmolarities +/- DDAVP (ADH) test +/- water deprivation (diabetes insipidus)
    • Treat cause and correct sodium (slowly- risk of osmotic demyelination)
      • if euvolaemic- give dextrose only rather than saline (and/or salt restrict)
      • if hypovolaemic- give saline (NB must replace fluid loss prior to sodium correction)
• Potassium (3.5-5.5mmol/l)
  • Hypokalaemia
  • Hyperkalaemia
• Calcium (corrected calcium 2.05-2.6mmol/l)
  • Hypocalcaemia
  • Hypercalcaemia
• Magnesium (0.75-1mmol/l)
  • Hypomagnesaemia
    • Causes
      • Excess loss e.g. diuretics, severe diarrhoea, DKA
      • Poor nutrition/alcoholism
        • NB most magnesium is found in bone and cells, so will reduce if calcium, phosphate and/or potassium are low (ALL OF THESE SHOULD BE CHECKED WITH MAGNESIUM)
    • Management
      • Replace Mg – 8-12g of magnesium sulphate (as an infusion) over first 24 hours then 4-6mg/day until Mg is normal
    • NB ALWAYS REPLACE MAGNESIUM PRIOR TO OTHER ELECTROLYTE DISTURBANCES (particularly hypocalcaemia, which will not correct itself without normalising Mg first)
• Phosphate
  • Hypophosphataemia
    • Causes
      • Vit D deficiency
      • Refeeding syndrome
      • Primary hyperparathyroidism
      • Poor nutrition/alcoholism
    • Management
      • Often can be managed with oral phosphate supplements if necessary

Hyperkalaemia

Background

• Normal potassium levels are quoted as 3.5-5mmol/l
• Regulated by a number of factors including
  • RAAS (aldosterone); acid base balance (acidosis can cause a hyperkalaemia as H+ and K+ ions compete at the Na-K exchange at the distal tubule; insulin
• Can be classified as
  • Mild 5.5-5.9mmol/l
  • Moderate 6-6.4mmol/l
  • Severe >6.5mmol/l

Causes

• Renal causes
  • Acute Kidney Failure
  • Chronic Kidney Disease (NB However, renal causes are generally failure to excrete K+; in CKD, excretion via the bowel can maintain a relatively normal K+)
  • Renal tubular acidosis
• Increased intake/circulation
  • Exogenous (supplementation)
  • Endogenous (tumour lysis syndrome; rhabdomyolysis; trauma; burns)
• Metabolic shift
  • Acidosis (H+ competes with K+ in the kidney for excretion) e.g DKA
• Drugs
  • Potassium sparing diuretics; ACE inhibitors; Angiotensin II receptor blockers; spironolactone; ciclosporin; cotrimoxazole; heparin (inhibition of aldosterone secretion); occasionally beta blockers (in renal failure); digoxin toxicity; suxamethonium; theophylline
• Pseudohyperkalaemia
  • Sample tube haemolysis; prolonged tourniquet time; wrong tube (potassium EDTA) etc
  • Dehydration
  • If in doubt, re-test

Presentation

• Weakness and fatigue may be the only symptoms.  Rarely, muscle paralysis/SOB, palpitations or chest pain
• Bradycardia may be present (heart block); tachypnoea can be present (respiratory muscle weakness)
• Depressed reflexes

Investigations

• U&Es +/- emergency potassium
• ECG (URGENT)
  • Tall-tented t-waves (often earliest sign)
  • Small P waves (occasionally also prolonged PR-interval)
  • Wide QRS complexes (which, when severe, may develop with t waves to produce VT/VF/asystole)

Acute Management

• For mild hyperkalaemia
  • ECG
    • If there are changes of hyperkalaemia, treat as severe
  • Assess fluid status
    • If hypovolaemic resuscitate with saline 0.9%
    • If euvolaemic consider slow IV 0.9% saline
    • If hypervolaemic give 50mg IV furosemide stat
  • Omit and drugs that may contribute to hyperkalaemia
  • Address any hyperglycaemia
  • Repeat K+ in 4-6 hours
    • If it remains high- give regular calcium resonium (15mg TDS/QDS)
• For moderate hyperkalaemia
  • 12-lead ECG and cardiac monitoring
    • If any changes, treat as severe
  • Assess fluid status
    • If hypovolaemic, resuscitate with saline 0.9%
    • If euvolaemix give slow IV saline 0.9% or sodium bicarbonate 1.26% (e.g. 500ml/4 hours)
    • If hypervolaemic, give 100mg furosemide IV
  • Give IV insulin according to bedside BM
    • <12
      • 10 units actrapid in 50mls of 50% dextrose (i.e. 25g glucose) over 10-15mins
      • Followed by 10% dextrose infusion (500ml/12 hours)
    • >12
      • 10 units actrapid in 50mls of 0.9% saline over 10-15 mins
      • Monitor BMs every 30 mins
      • Once BM <12 give 10% dextrose infusion as above
  • Repeat K+ measurement 30 mins after every insulin infusion
  • Review and change any medication that may be contributing
• For Severe Hyperkalaemia
  • 12-lead ECG and cardiac monitoring
  • Give 10ml of 10% Calcium Gluconate as an IV bolus over 10 minutes
    • Repeat every 5 mins until ECG changes no longer present and every 30 mins if K+ is still >6.5mmol/l
  • Give IV insulin as for moderate hyperkalaemia
  • Also give nebulised salbutamol 10mg stat (unless HR >130bpm)
    • (NB give 20mg if patient takes a regular beta blocker)
  • Assess fluid status and manage identical to moderate hyperkalaemia
  • Repeat K+ measurements at least every 30 mins
• NB If the patient doesn’t respond to diuresis; initial potassium lowering therapy or if they patient has associated AKI OR CKD, patients should be transferred to HDU and the renal team contacted (+/- consideration for dialysis)