Care of the surgical patient II Flashcards
early warning scores (EWS)
help with ‘flagging up’ patients for urgent medical assessment and monitoring response to treatment.
which aprameters does NEWS look at
- respiration rate
- oxygen saturation
- systolic blood pressure
- pulse rate
- level of consciousness or new confusion (AVPU)
- temperature.
reaction to EWS
- low score – increased frequency of observations and nurse in charge notified;
- medium score –urgent call to patient’s primary medical team;
- high score – emergency call to medical emergency team/critical care outreach team.
define sepsis
life threatening organ dysfunction due to dysregulated host reponse to infection
septic shock
sepsis with hypotension, despite adequate fluid resuscitation or requiring the use of inotropic agents to maintain a normal systolic blood pressure.
lactate >2
Management usually involves aggressive fluid resuscitation and antibiotic therapy, with the likely involvement of the critical care team. Inotropes are often used to maintain organ perfusion.
screening tools for sepsis
SOFA and qSOFA
qSOFA parameters
RR >22
BP <100mmHg systolic
altered mental state
red flags for sepsis
sources of ifnection for sepsis
- Urine dip +/- culture
- Chest X-ray (CXR)
- Swabs (e.g. surgical wounds)
- Operative site assessment (via CT or US imaging)
- Cerebrospinal fluid sample (via LP)
- Stool culture
Sepsis on surgical wars
The common sources of pyrexia in a surgical patient can be remembered using the Seven C’s:
- Chest (infection)
- Cut (wound infection)
- Catheter (UTI)
- Collections (abdomen, pelvic etc.)
- Calves (DVT)
- Cannula (infection, if applicable)
- Central line (infection, if applicable)
manageemnt of sepsis
sepsis 6
BUFALO
B- blood culture
U- urine output
F- give fluids
A- antibiotics (IV)
L- measure lactate
O- oxygen
when to escalate management in a sepsis patient
- Evidence of septic shock
- Lactate > 4.0mmol
- Failure to improve from initial management
where to get ABG from
- Can use arterial lines
- Or take blood from the radial artery
types of respiratory failure
- Low PaO2 indicates hypoxia and respiratory failure
- Type 1- Normal pCO2 with low PaO2
- Type 2 -Raised pCO2 with low PaO2
reading ABG
- Look at PaO2- is the patient hypoxic
- Look at the pH (acid-base balance)
- Is the cause respiratory or metabolic?
Look at PaO2- is the patient hypoxic
- PaO2- amount of O2 dissolved in blood
- Check FiO2 (fraction of inhaled oxygen)
- Room air has a FiO2 of 21%
- Venturi masks used to control FiO2
Look at the pH (acid-base balance)
- Low- acidic
- High- alkalotic
causes of respiratory acidosis
Raised PaCO2- suggests patient is retaining CO2
- COPD (blue bloater)
- life threatening asthma attack (tired)
causes of respiratory alkalosis
- Low PaCO2- blowing off CO2 (hyperventilation- i.e anxiety)
causes of metabolic acidosis
Low pH due to low bicarbonate
- Raised lactate (tissue hypoxia e.g. sepsis)
- Raised ketones
- Raised H+
- Reduced bicarbonate
- diarrhoea, renal failure or type 2 renal tubular acidosis
causes of metabolic alkalosis
Raised pH due to raised bicarbonate or reduced H+
- Kidneys- increased aldosterone
- Primary hyperaldosteronism
- Reduced H+ ions
- GI loss- vomiting (HCL)
- Kidneys- increased aldosterone
- Primary hyperaldosteronism
- Liver cirrhosis
- HF
- Loop and thiazide diuretics
- Liver cirrhosis
- HF
- Loop and thiazide diuretics
hyperaldosteronism and metabolic alkalosis
Hyperaldosteronism – Loss of hydrogen ions in the urine occurs when excess aldosterone (Conn’s syndrome- hyperaldosteronism) increases the activity of a sodium-hydrogen exchange protein in the kidney
Three major groups of pain
- Post op pain
- Injured infected or inflamed
- Patients with chronic pain
essential pain management
- RAT system
-
Recognise
- What patient is saying
- Signs:
- Hypertentsion
- Tachycarida
- GI symptoms
- Behavioural changes e.g. withdrawal, resp changes
-
Assess
- Take pain history (SOCRATES)
- Pain scores appropriate to patient
- Verbal analogue scale
- Faces pain scale (FPS)
- Good for kids
- Treat
methods of quantifying pain
two mechanisms of pain
nociceptive
neuropathic
nociceptive pain
more physiological
- Tissue injury
- Protective function e.g. moving hand away from sharp object
- Description
- Sharp
- Well localised
- Deep somatic pain- dull ache poorly localised
- Visceral- localised and more autonomic stimulation
neuropathic pain
more pathological
- Pain caused by disease of the sensory nervous system
- Diabetic neuropathy, phantom limb pain, sciatica
- Tissue injury may not be obvious
- Does not have a protective function
- Description
- Burning, shooting, pins and needles, numbness
- Not well localised
- Diabetic neuropathy, phantom limb pain, sciatica
two main sensory pathways (ascending)
dorsal column-medial leminscus system
spinothalamic system
The dorsal column-medial lemniscus system
- System the CNS uses to carry info to the brain concerned with
- fine touch
- 2 point discrimination
- vibration
- (not as important for survival as the spinothalamic system)
spinothalamic system
- Ancient system responsible for survival of organisms
- Concerned with
- Pain
- Temperature
- Pressure/crude touch
outline the dorsal column-medial lemniscus system
e.g. detecting vibration in a lumbar dermatome
- Receptor in lumbar dermatome communicates with first order sensory neurone (cell body in dorsal root ganglion) and projects into the spinal cord
- First order neurone ascends up the SC to the medulla of the spinal cord, where it synapses onto a second order neurone
- Second order neurone decussates (cross the midline) and ascends all the way up to the thalamus and synapses onto third order neurone
- Medial lemniscus- pathway connecting the gracile and cuneate nuclei with the thalamus
- Third order neurone projects to the sensory cortex
- Lumbar region of the somatosensory cortex found medially
outline the spinothalamic system
e.g. detecting pain in the lumbar region
- Receptor in lumbar dermatome connects to first order neurone
- Synapses with second order neurone at approx. the level it enters (dorsal horn)
- Second order neurone decussates (crosses midline) and ascends up the cord (spinothalamic tract) into the brainstem and into the thalamus
- In the thalamus the second order neurone synapses with third order neurone which projects to the medial part of the primary sensory cortex (lower body)
e.g. detecting pain in the cervical region
- Receptor in cervical dermatome connects to first order neurone
- Synapses with second order neurone at approx. the level it enters (DH)
- Second order neurone decussates (crosses midline) and ascends up the cord (spinothalamic tract) into the brainstem and into the thalamus
- In the thalamus the second order neurone synapses with third order neurone which projects to the lateral part of the primary sensory cortex (upper body)
pain transmission through spinothalamic tract
- Peripheral tissue injury causes release of lots of different chemical markers e.g. substance P
- Nociceptive (pain receptors) stimulated by chemical markers
- Signals travel in Adelta (myelinated- fast transmitting) or C nerve (slow transmission) to spinal cord (first order nerves)
- First order nerves synapses upon second order neurone in the dorsal horn of the grey matter (lamina I and II)
- Second order neurone decussates (crosses) at around the level the first order neurone enters the CNS
- Ascends up the spinothalamic tract and synapses with third order neurone in the thalamus
- Third order neurone synapses into somatosensory cortex (also limbic systema nd brains tem)
- Brain perception occurs in the brain
regulation of pain transmission
-
Why does rubbing a painful area of a body relieve some of the pain e.g.
- You stub your toe
- Pain is detected by C-fibres (nociceptive first order neurones) and carried up via the spinothalamic tract up to the somatosensory cortex of the brain- PAINNNNNNNN
- You start rubbing the sore toe
- Mechanoreceptors detect rubbing movement – ABeta (AB) neurones project into the dorsal horn and synapse mainly with interneuron instead of secondary neurones
- When an interneuron is stimulated it can start inhibiting second order neurones which are sending pain signals up to the somatosensory cortex
-
How can people deal with extreme pain? e.g. hypnosis and extreme trauma can reduce pain experienced
-
Due to descending modulation which inhibits pain pathway
- Hypnosis activates cortical neurones which project down to the midbrain
- These excitatory neurones stimulate neurones in the periaqueductal grey (PAG)
- These activated PAG neurones can project down into the medulla where they are able to stimulate neurones in the nucleus raphe magnus (large nucleus near the midline- part of reticular formation)
- NRM neurones descend down the cord where they have an inhibitory effect on the second order sensory neurone by stimulation the inhibitory interneurons
-
Due to descending modulation which inhibits pain pathway
management of neuropathic pain
split into pharmacological and non-pharmacologcial
non-pharmacological treatment of neuropathic pain
CBT
transcutaenous electric nerve stimulation
capsaicin cream (for localised pain)
pharmacological management of neuropathic pain
gabapentin
amitripyline
pregabilin
paracetamol
action: analgesic and antipyretic (mild to mod pain)
pharmacokinetics: inactivated by conjugation in the liver
liver metabolism of paracetamol
- At normal therapeutic dose paracetamol intermediate (NAPQI) is conjugated with glutathione
- Hepatic glutathione is limited so if too much paractemol taken, build up of NAPQI- TOXIC)
paracetamol overdoese
- Nausea, vomiting and abdominal pain – first 24 hours
- Maximal liver damage occurs at 3-4 days
- Due to accumulation of NAPQI (not enough glutathione to power phase 2 reaction)
- Therefore NAPQI starts causing necrosis of cells esp in the liver
-
Treatment
- Activated charcoal- only of use if paracetamol overdose recently taken
- Lethionine (oral drug)
- Glutathione thiol replacement – IV N- acetylcysteine
NSAIDS
action: analgesic and anti-inflammatory
MOA: COX- inhibitors, reducing prostaglandins, prostacyclins and thromboxane synthesis (which is good and bad)
analgesic action of ASAIDS
reduces amount of arachidonic (made from dietary linoleic acid) acid converted into PGE2 (which causes pain- prostaglandin)
inflammatory action of NSAIDS
- During inflammation ↑COX activity → prostaglandin mediated increase in vasodilatation and oedema
- NSAIDs reduce production of prostaglandins released at site of injury
- Vasodilation in post capillary venules contributes to increased permeability and local swelling- NSAIDs inhibit this
- Symptomatic relief with COX inhibition – little effect on underlying chronic condition (wont cure just helps with inflammation)
contraindication of NSAIDS
- Renal function
- NSAIDs produce reverisble decrease in GFR and decreased renal blood flow due to reduced amount of PGE2 which causes vasodilation
- GI disease e.g. peptic ulcers (give PPI cover)
- Asthma
selective COX-2 inhibirirs
e.g. Celecoxib
- Less inhibitory action on COX-1 but selectivity for COX-2 varies among drugs
- Less GI ADRs, renal ADRs similar to non-selective
- Do not share antiplatelet action
- But inhibit PGI2 - potentially leading to unopposed aggregatory effects – CVS risk problem
- Some evidence of less analgesic effect
- Can be useful when monitored in severe osteo and rheumatoid arthritis for longer term treatment – reduced GI side effects
- ALL NSAIDs increase risk of MI including in low risk people (↓PGI2 in coronary vasculature?)
- Reduced cycloprotective of the CVS by removing PGI2 etc
opioids MOA
- Agonist binds to MOP (U) receptor
- Leads to decrease in cAMP
- Efflux of potassium
- Hyperpolarisation of membrane
- Decreases substance P and GABA release
- Increases dopamine release
examples of opioids
all strong pain killer
fentanyl
- strongest agonsit of U receptors
morphine
- strong agonist of U receptor
codeine
- moderate agonsit of U receptor
Buprenorphine
- partial agonist
adverse drug reactions to opiots
- respiratory depression (do not give if drunk or head injury)
- nausea and vomiting
- constipation
naloxone
-
Opioid antagonist
- competitive antagonism of opioid at U receptor
-
Uses
- Rapidly reverse opioid overdose
- short half life
- may need to be given again soon after
VTE prophylaxis
DVT and PE
