Compartment syndrome and rhabdomyolysis and pain management

Question 1

Scenario: 28 yr old male, leg crushed for a few hours, left unobserved on orthopaedic ward. Bloods: AKI. Urine dip: blood.

What are the complications?

Answer 1

-Compartment syndrome
-Rhabdomyolysis

Question 2

What is the clinical picture of compartment syndrome?

Answer 2

-Worsening pain: this may be out of proportion to the injury
-Paraesthesia: especially the loss of two point tactile discrimination

Clinical signs
–> tense and swollen compartments
–> sensory loss
–> pain on passive stretching

Loss of regional pulses which is a LATE sign

Question 3

How to diagnose compartment syndrome in a patient with altered sensorium or sensorimotor deficit

Answer 3

This can be achieved by:
–> measurement of intercompartmental pressure, tissue pressures of >30mmhg suggest decreased capillary blood flow, which can result in muscle and nerve damage from anoxia
–> blood pressure: the lower the systemic pressure, the lower the compartment pressure that causes compartment syndrome

Question 4

What is a normal compartment pressure?

Answer 4

0-15mmhg
If >30, indication for fasciotomy

Question 5

What is the treatment for compartment syndrome?

Answer 5

Emergency fasciotomy e.g. in lower leg 4 compartment fasciotomies through 2 incisions as an emergency procedure

Question 6

What will you say to the patient when you consent for fasciotomies?

Answer 6

-Explain operation, complications (permanent nerve damage, permanent muscle damage, permanent scarring, loss of affected limb, infection, kidney failure, in rare cases death

Question 7

Why would you get acute renal failure in compartment syndrome?

Answer 7

–>Rhabdomyolysis
–>accumulation of myoglobin in renal tubules leads to tubular obstruction
–> formation of obstructive casts with uric acid
–> low blood pressure can lead to renal arteriole vasoconstriction and relative reduced blood flow
–> together these processes lead to ATN

–> nephrotic effect of myoglobulin precipitating in renal tubules
–> decrease extracellular volume –> vasoconstriction
–> renal tubular ischaemia and necrosis
–> myoglobulin, uric acid –> obstructive cast formation

Question 8

What is myoglobin?

Answer 8

-O2 binding protein found in muslces

Question 9

What is the definition of rhabdomyolysis?

Answer 9

-The release of potentially toxic muscle cell components into the systemic circulation

Question 10

What are the causes of rhabdomyolysis?

Answer 10

-Blunt trauma to skeletal muscle e.g. crush injury
-Massive burns
-Hypothermia or hyperthermia
-Ischaemic reperfusion injury e.g. clamp on artery during surgery
-Prolonged immobilisation on hard surface
-Strenuous and prolonged spontaneous excercise e.g. marathon running
-Drugs e.g. statins, fibrates, alchohol

Question 11

What are the biochemical results in rhabdomyolysis?

Answer 11

-Increased CK >5 times normal
-Increased lactate, LDH, creatinine
-Electrolyte disturbances:
—> hyperkalaemia (and metabolic acidosis with increased anion gap)
—> hypocalcaemia(myocyte necrosis is associated with calcium influx into cell)
–> hyperphosphataemia
–> hyperuricaemia

-Myoblobinuria suggested by positive dipstick to blood in abscence of haemoglobinuria (red cells on microscopy)

Question 12

What is the managementof rhabdomyolysis

Answer 12

-ABC
-> fluid resus: ensure good hydration to support UO >300ml/hr using IV crystalloid until myoglobinuria has ceased
–> diuretics (manittol) may be used
–> alkalinisation of urine: NaHCO3 to prevent renal damage
–> treat electrolyte disturbance (hyperkalaemia
–> monitor ECG, electrolytes,

NaHCO3:
–> tamm horsfall protein precipitates at lower ph, so prevents cast formation

Question 13

Define pain

Answer 13

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

Question 14

What are the side effects of opioids?

Answer 14

-Respiratory depression
-Nausea/vomiting
-Constipation
-Urinary retentaion

Chronic use
-Hypogonadism
-Immunosuppression
-Withdrawal

Question 15

What is the pain pathway?

Answer 15

Pain is tramsmitted via fast A-delta fibers (sharp pain) and slower C fibers (dull pain) to lateral spinothalamic tract and then to thalamus

Question 16

What is patient controlled analgesia?

Answer 16

-Syringe pump connected IV to allow patient to self-administer boluses of morphine
-Overdosage is avoided by limiting size of bolus and frequency of administration
-Lock out time is set within which pressing the button again will not result in a bolus of analgesia
-One way valve preventing backflow of opiates into the infusion chamber which may lead to overdose when redelivered

Question 17

What is normal dose of morphine pca?

Answer 17

0.5-2mg bolus

Question 18

What are the disadvantages of a PCA?

Answer 18

-Patient has to be alert and orientated to use it
-Can break down, run out of battery
-Sleep disturbance
-Limits patient mobility

Question 19

What are the complications of pain?

Answer 19

CVS
-Increased HR, BP, myocardial consumption –> increased risk of MI
-DVT from immobility

GIT
-delayed gastric emptying
-Reduced bowel motility
-Paralytic ileus

Respiratory
-Limits chest movements leading to atelectasis, retained secretions, pneumonia

Question 20

How would you manage patient in post op pain?

Answer 20

-A-E assessment
-Assess severity with pain scale
-Give analgesics according to WHO ladder with regular assessment

Non pharmacological methods:
–> cold or heat
–> Immobilisation of injured limbs
–> TENS`

Question 21

Give examples of opioids in common use. Which are synthetic and which are non synthetic?

Answer 21

-Non synthetic: morphine, codeine (10% metabolised to morphine)
-Semi-synthetic: diamorphine, dihydrocodeine
-Synthetic: pethidine, fentanyl

Question 22

Why is codeine bad?

Answer 22

-Drowsiness, constipation, orthostatic hypotension
-CYP2D6 enzyme converts codeine into morphine in the liver
-Some patients have high levels of this enzyme, resulting in rapid metabolisation to morphine, causing over-intoxication which can cause respiratory depression
-Some patients have less of this enzyme and therefore lose analgesic affect while still suffering side effects

Question 23

What is the mechanism of action of paracetamol?

Answer 23

-Mechanism poorly understood
-Generally considered to be weak inhibitor of prostaglandin production
-In vivo effects similar to COX 2 inhibitors

Question 24

How would you manage paracetamol toxicity?

Answer 24

-Activated charcoal 30mins-2 hrs ingestion
-Acetylcysteine: antidote replenishing body stores of antioxidant glutathione
-Liver transplant in acute liver failure

Question 25

What different pain scoring systems are there?

Answer 25

-Verbal numerical rating scale 0-10
-Visual anaglogue scale (mark on 10cm line no pain to worst imaginable)
-Wong-baker FACES (children)

Question 26

What is epidural anaesthesia?

Answer 26

Epidural anaesthesia is a form of regional anaesthesia that involves injection/infusion of anaesthetic medidcation into epidural space

Question 27

What are features of an epidural?

Answer 27

-Drug injected into epidural space
-Can be performed at any level along spinal column
-Slow onset (15-25 minutes)
-Large volume (10-20ml) LA +/- opioids
-Large needle (16G) used
-Usually epidural catheter is inserted for repeated doses or infusions

Question 28

Spinal features:

Answer 28

-Drug injected into subarachnoid space
-Can be performed at level below termination of spinal cord
-Rapid onset (usually <5 minutes)
-Small volume (2-4ml) LA +/- opioids
-Single shot given with thin needle (25G)

Question 29

What are diffeneces between epidural and spinal?

Answer 29

-Space injected (Epidural vs subarachnoid)
-Level performed (any level vs below termination)
-Onset (slow vs rapid)
-Volume injected (large vs small)
-Needle used (large vs small)
-Number of infusions (multiple vs few)

Question 30

Describe layers encountered when inserting needle into epidural space

Answer 30

-Skin
-Subcut fat
-Supraspinous ligament
-Interspinous ligament
-Ligamentum flavum

Question 31

Describe the effects of epidural analgesia

Answer 31

Sympathetic block of transmission of signals through nerve roots near the spinal cord

Question 32

How can epidurals cause bradycardia?

Answer 32

-‘High epidural block’: spread of LA affecting spinal nerves above T4
-blocks cardio-accelerator fibres
-Leads to unopposed parasympathetic action of vagus nerve

Question 33

What is a high epidural block?

Answer 33

-Results from excessively large dose of local being injected into epidural space
-Spread of LA affecting nerve roots above T4
-Hypotension, sensory loss or paraesthesia high thoracic/cervical nerve roots
-Bradycardia: blocking of cardio-accelerator fibres leading to unopposed parasympathetic cardiac innervation via vagus nerve
-Dyspnoea due to blockade of nerve supply to intercostals + diaphgragm

Question 34

How would you assess level of epidural blockade?

Answer 34

-Pain and temp are conducted by same nerve fibre types
-Therefore the only appropariate test is to assess ability to detect cold stimulus which is impaired in blocked dermatomes with either ice or ethyl chloride spray

Question 35

How do you treat hypotension resulting from epidural block? What is mechanism behind hypotension?

Answer 35

-Pt is hypotensive due to vasodilatation secondary to sympathetic block
-Stop epidural
-IV fluid resuscitation
-Vasoconstrictor drugs: metaraminol

Question 36

What is the mechanism of high epidural block induced bradycardia? How is it treated?

Answer 36

-Cardio-accelerator fibres originate between T1-T3. Epidural/spinal blockade results in bradycardia from unopposed parasympathetic (vagal) tone
-This is treated with atropine or glycopyrrolate
-Sometimes adrenaline, dobutamine or isoprenaline may be needed

Question 37

Describe the WHO analgesic ladder

Answer 37

-Mild pain: simple oral analgesics e.g. paracetamol, NSAIDs
-Moderate pain: combined therapies, oral weak opioids eg. tramadol, codeine
-Strong pain: opioids +/- oral analgesics e.g. IV/IM opioids, PCA
-Epidural