Critical Care Flashcards
Location of base of skull fractures
75% are posterior fossa (temporal / occipital bones)
25% are anterior fossa (frontal /sphenoid / ethmoid bones)
Posterior fossa fracture signs
Battle’s sign – bruising over the mastoids
CSF Otorrhoea
Bleeding of the ear
Conductive deafness
=> Lasts 6-8 weeks
CN palsies of V, VI, and VII
=> Facial numbness and/or weakness
=> Lateral rectus muscle palsy
Base of skull fracture - Mx
POSTERIOR FOSSA - patients should be referred to neurosurgery, but often will not require intervention.
ANTERIOR FOSSA - patients require urgent referral to neurosurgery
Anterior Fossa Fracture signs
Raccoon eyes – bruising around the eyes
CSF rhinorrhoea
Bleeding from the nose
Complications of base of skull fractures
Intracranial infection
=> Prophylactic ABX are given for 7 days after any CSF leak has ceased.
Facial nerve palsy
Ossicular chain disruption
Carotid injury
Depressed skull fractures
Can be subtle on examination
Impossible to know if there is interruption of the dura without exploration
All compound depressed skull fractures are surgically explored within 12 hours.
Initial management of cardiac arrest
- Patient unresponsive and not breathing normally.
- Initiate CPR 30:2
- Call resus team
- Attach defibrillator and monitor
- Gain IV access - Assess rhythm (halt compressions for 5 seconds)
- Shockable = VF, pulseless VT
- Non-shockable = PEA, asystole
- Return of Spontaneous circulation
Cardiac Arrest - Management of shockable rhythms
Resume compressions, charge the defibrillator.
Stop compressions and deliver shock
=> Immediately resume compressions
After 2 mins, re-assess the rhythm
=> Deliver another shock, if shockable
=> Immediately resume compressions
After 3 shocks, administer adrenaline and amiodarone
- Adrenaline 10mL 1:10,000 IV
- Amiodarone 300mg IV
Repeat adrenaline every 3-5 minutes.
What are non-shockable rhythms?
Asystole
Pulseless Electrical Activity (PEA)
Asystole
the heart’s electrical system has shut down and there is no heartbeat.
Can be the result of untreated VT or VF.
CPR should be initiated immediately to provide the best chances of survival.
If an Asystole rhythm is detected by an AED, it will not shock the patient, as defibrillation is not a viable treatment here.
Pulseless Electrical Activity (PEA)
the heart’s electrical activity is too weak to continue pumping blood throughout the body.
An AED will not correct this arrhythmia, and CPR should be administered as soon as possible to provide the best patient outcome
Cardiac Arrest - Mx of non-shockable rhythms
Give 10mL 1 in 10,000 adrenaline IV as soon as access secured.
Continue 30:2 compressions until the airway is secured (i.e. with advanced airway).
=> Once the airway is secured, do not stop compressions for ventilation.
Recheck rhythm after 2 minutes:
=> If compatible with cardiac output, check for a pulse or signs of life.
=> If no pulse/signs of life, continue CPR
=> Recheck rhythm at 2 min intervals
Give further adrenaline every 3-5 mins (i.e. every 2 cycles of CPR)
If the rhythm becomes shockable, move to that side of management.
Post-cardiac arrest syndrome
- Post-arrest brain injury
- Post-arrest myocardial dysfunction
- Systemic ischaemia / reperfusion response
- Persistent precipitant pathology
The severity of the syndrome depends on the duration of the arrest, or it may not happen at all.
Good post-arrest management is vital to reduce the severity.
Post-arrest Care - A & B
If arrest was brief, Pt won’t need intubation/ventilation
Give O2 if sats <94%
Avoid unnecessary aggressive O2 therapy
Any patient with reduced cerebral function should be sedated and ventilated, with admission to ICU.
Post-arrest care - C
If there is ST elevation / LBBB on ECG, PCI is indicated, even if they remain comatose and ventilated.
Perform echo to assess the extent of myocardial dysfunction
Patients will often require ionotropic support initially
=> Titrate ionotropic support/fluids to maintain adequate urine output.
There is often transient hypokalaemia
=> may need IV potassium to maintain levels.
Post-arrest care - D
In most patients, cerebral auto-regulation is lost following arrest, so maintain BP near to MAP.
EEG may be required to detect seizures in sedated patients (these should be treated appropriately).
Post-arrest care - E
A period of hyperthermia is common in the first 48 hours after arrest (associated with poor outcomes)
Targeted temperature management:
- Cooling to 36 degrees is neuro-protective (reduces inflammatory response to hypoxia).
- Indicated for those who remain unresponsive following ROSC.
- Sedation is required to prevent shivering
- Cool for >24 hours.
How is targeted temperature management done?
Cooling blankets, pads, or intravascular heat exchangers can be used
Sedation is required to prevent shivering
Cool for >24 hours.
What are the aims of post-arrest care
A-E assessment
Maintain O2 sats of 94-98%
Find and treat precipitating cause of the arrest.
Primary vs Secondary traumatic brain injury
Primary – as an immediate result of brain trauma
Secondary – develops later as a result of complications (hypoxia, ischaemia, haematomas).
Primary brain injuries
Concussion
Diffuse Axonal Injury
Focal Brain Injuries
Concussion
= Transient loss of consciousness but no persistent neurological signs
Temporary confusion can occur
May be signs of neurological injury on CT
Diffuse axonal injury
Visible on high-resolution CT
The number of axons damaged increases with severity of injury
Does not cause raised ICP
Tx = supportive
Can cause sequelae of deficiencies in higher function
* Loss of concentration / memory disturbances
* Personality changes
What are Focal Brain Injuries?
= Gross damage to localised areas of the brain, visible on CT
- Coup injuries – beneath the site of impact
- Contre-coup injuries – on the opposite side of the brain, due to rebound within the skull.
- Haemorrhage / haematoma
These can all act as space-occupying lesions and can result in secondary brain injuries
Post-concussion syndrome
50% of those suffering a head injury will suffer long-term disability
Classic problems:
- Dizziness
- Headache
- Poor concentration/memory
- Inability to work & difficulties with self-care
Specialist follow-up is advised following all severe head injuries
Assessment of a patient with a head injury
C-spine precautions
ABCDE resuscitation
- A – guedel airway or intubation usually required (record GCS prior to intubation)
- B – chest injuries often co-exist, and can lead to secondary brain insults (hypoxaemia is an indication for intubation)
- C – often polytrauma patients, leading to shock (XM is vital)
Record GCS
Brief history if conscious
=> Any seizures? Lucid Interval? Intoxicated?
Neurological Examination
Appropriate Imaging:
- CT head if indicated
- C-spine radiography if indicated (always indicated in head trauma with LoC)
Prevent secondary insults
=> Monitor Pt with blood gases and BP
Signs of Neurological Deterioration in a patient with a head injury
Falling GCS = most important sign
Changing pupillary size / responsiveness
Development of focal neurological signs
Changing respiratory rate
=> Irregular respiration, or bradypnoea
Falling pulse, rising BP
=> Cushing’s Reflex – late sign
=> Due to pressure on the medulla oblongata
=> More common in younger patients
Cushing’s reflex
= Falling pulse, rising BP
a late sign
Due to pressure on the medulla oblongata
More common in younger patients
Blood Gas Derangement in head injury patients
Hypercapnia leads to increased cerebral vasodilation
=> This increases cerebral blood volume, and thus raised ICP
=> Patients with raised ICP may be hyperventilated on ICU to reduce PaCO2
Hypoxaemia can also cause cerebral vasodilatation
=> Also leads to particularly rapid lactic acidosis within cerebral neurones, which causes cerebral damage.
Hypotension in head injury patients
Under physiological circumstances, cerebral blood flow is autoregulated with MAP lies between 60-160 mmHg
Following a head injury, this autoregulation is lost and cerebral blood flow relies on SBP
As such, resuscitation is vital to maintain SBP
Head injury - stable patients
Stable patients with a GCS of 15 can be safely discharged.
If they have had a period of LoC after head trauma, skull XR will be performed
Discharge with a head injury warning card
If intoxicated, they generally need to be admitted as it is impossible to tell whether it is the alcohol or head injury responsible for the Sx
head injury - what are indications for head CT within 1 hour of arrival?
GCS <13 at any time, or <15 two hours after the injury
Focal neurological deficit
Signs of increasing ICP
Suspected skull fracture
Post-traumatic seizure
Vomiting on >1 occasion
head injury - what are indications for head CT within 12 hours of arrival?
Anticoagulated patients (or other known coagulopathy)
LoC plus:
- Age >65
- Dangerous mechanism of injury (e.g. fall from great height)
- Retrograde amnesia >30 minutes (inability ro recall the events immediately before injury)
Head injury - when to admit
If imaging shows pathology
If GCS <15 (monitor every 30 mins until it is)
Continuing worrying signs/sources of concern
Reversible causes of cardiac arrest
4 H’s:
Hypokalaemia / hyperkalaemia
Hypothermia
Hypovolaemia
Hypoxia
4T’s:
Tension PTX
Tamponade
Toxins
Thrombosis
What is shock?
= acute circulatory failure that compromises tissue perfusion.
Triad of signs in shock
- Signs of reduced perfusion
* Prolonged capillary refill time
* Reduced urine output
* Altered mental state. - Low BP
* Usually by at least 40mmHg - Raised lactate
* Anaerobic respiration produces lactate, which accumulates in the blood, causing a hyperlactataemia.
Mean Arterial pressure
= DBP + (SBP-DBP)/3
How to calculate:
BP
CO
SV
BP = Cardiac Output x Systemic Vascular Resistance
CO = Stroke Volume x HR
SV = End Diastolic Volume – End Systolic Volume
Hypovolaemic Shock - pathophysiology
Occurs when there is insufficient volume of blood in the intravascular compartment.
Causes - haemorrhage (revealed or concealed), dehydration
Distributive Shock - pathophysiology
Occurs when there is failure of vasoregulation (i.e. a problem with the systemic vascular resistance).
Causes - sepsis, anaphylaxis, neurogenic
Cardiogenic Shock - pathophysiology
Occurs when the heart stops pumping effectively.
Causes = DIRECT pump failure – e.g. MI, arrythmias, valve dysfunction, metabolic disturbances
Obstructive Shock - pathophysiology
Occurs when there is blockage of blood flow, either in a great vessel or of the heart itself.
Causes = INDIRECT pump failure – massive PE, cardiac tamponade, tension PTX
Effects of shock on cerebral perfusion
Autoregulation with MAP of 50 – 150 mmHg
Below this threshold the patient will become agitated, confused, drowsy, and eventually unresponsive.
Effects of shock on the heart
Reduced diastolic pressure leads to inadequate myocardial perfusion,
=> leading to ischaemic chest pain, arrythmias, and eventually infarction
Effects of shock on respiratory system
Increased respiratory rate due to metabolic acidosis
Effects of shock on renal system
Autoregulation with MAP of 70-170 mmHg
Below this, there will be oliguria which ultimately leads to impaired renal function (due to toxin build-up)
Effects of shock on GI system
Decreased gut motility and nutrient absorption, and decreased ability to sustain normal flora, leading to infection susceptibility
Effects of shock on the skin
Blood supply is centralised, giving cool / clammy / mottled peripheral skin
what is Septic Shock ?
= severe sepsis with hypotension not responding to fluid resuscitation
A mixed picture – bacterial endotoxins have an effect of:
- Widespread vasodilatation (causing distributive shock)
- Increasing vessel permeability (causing hypovolaemia through third-space losses)
What is the management of septic shock?
SEPSIS 6 , including fluid resuscitation
urgent senior review
Crit care input if not responding to Tx
Anaphylactic shock
A type I IgE-mediated hypersensitivity reaction, occurring in response to an antigen that the body has already bene sensitised to.
Degranulation of mast cells => histamine release => profound vasodilatory effect => DISTRIBUTIVE shock
Another effect of Histamine = increased permeability of the vessels, leading to excessive third-space losses => HYPOVOLAEMIC shock.
This is compounded by bronchoconstriction and laryngeal oedema.
Management of Anaphylactic Shock
A-E Management:
- Secure airway (intubation if obstruction imminent)
- Remove the trigger
- Adrenaline 0.5mg IM (0.5 mL of 1:1000)
- Repeat every 5 mins if necessary
=> Acts as a vasopressor and decreases vessel permeability. - Chlorphenamine 10mg IV
- Hydrocortisone 200mg IV
=> Reduces the likelihood of biphasic anaphylaxis (i.e. a second event) - If wheeze, treat as per acute asthma.
- Raise the feet of the bed to help restore circulation (may need to give IV fluid bolus)
- Interval bloods for serum tryptase and histamine to confirm diagnosis.
Consider – ITU admission, longer-term need for epi-pen and skin-prick testing.
Hypovolaemic shock - Initial Management
Initial Management (A -> E):
Try to identify cause of fluid loss and replace fluid equivalent to the fluid being lost.
Titrate fluid to HR/BP/ CVP/ urine output response
Rapid boluses (250-500mL) with observation of response should be used
=> The fluid should ideally be warmed.
Vasopressors should be considered if persistently hypotensive.
Permissive hypotension should be used in haemorrhagic shock, titrating the SBP to 60-70mmHg (95-100 if there is a head injury)
=> Tranexamic acid is shown to increase major haemorrhage survival.
Categorising Haemorrhagic Shock
There is a relationship between the volume of blood loss and the signs and symptoms that are observed.
Class 1 = <750 mL
Class 2 = 750 - 1500 mL
Class 3 = 1500 - 2000 mL
Class 4 = >2000mL
BP may not be low until class 3 or 4
HR and RR increase with each class
Urine output (mL/hour) decreases with each class
Haemorrhagic shock - Mx
In cases of haemorrhagic shock, rapid blood loss or impending haemorrhagic shock, then the major haemorrhage protocol should be activated (2222).
=> This will enable the rapid delivery of packed cells, FFP and platelets
Cardiogenic shock - Mx
Initial management (A-E):
IV diamorphine 2.5 mg IV for pain/anxiety / breathlessness
Assess for pulmonary oedema, DO NOT give fluids.
Furosemide infusion can provide some relief in pulmonary oedema.
Likely to need ITU/CCU management for consideration of CVC/art line and ionotropic support.
What is neurogenic shock?
= Inhibition of sympathetic outflow from the spinal cord, leading to vasodilation.
Can occur due to epidural anaesthesia, or spinal cord injury above T6.
Presents with hypotension and bradycardia not responding to fluid resuscitation, so consider if there is a mechanism of spinal injury.
Treatment:
=> Likely to require fluid resuscitation and vasopressors.
Neurogenic shock vs spinal shock
Spinal shock is a transient “concussion” of the spinal cord, leading to flaccid areflexia that resolves as soft tissue swelling decreases.
=> There may be priapism, and there will be no reflexes below the level of injury.
What is sepsis?
= a life-threatening organ dysfunction due to a dysregulated and overwhelming response to infection.
Recognising sepsis
a NEWS2 score of 5 or more should trigger a sepsis screen, in the presence of:
- One of the risk factors:
- Extremes of age (<1 or >75)
- Impaired immune system (chemotherapy, comorbidities, long-term steroids).
- Recent invasive procedure (e.g. surgery, trauma, etc.)
- Broken skin (indwelling lines, IVDU, cuts/burns/blisters) - Otherwise unexplained concern from a HCP, carer or advocate.
RED sepsis - signs
- Objective evidence of new or altered mental state
- Systolic BP ≤90 mmHg, or a drop of >40 mmHg from the patient’s normal
- Heart rate ≥130 beats per minute
- Respiratory rate ≥25 breaths per minute
- Requirement for Oxygen supplementation to maintain sats
- Skin signs – such as a non-blanching rash, mottled or ashen appearance, or cyanosis
- A Lactate level of 2 or higher
- Recent chemotherapy
- Anuria for 18 hours, or <0.5ml/kg/hr if catheterised
AMBER sepsis - signs
These criteria mostly match up with the red flag criteria, with a lower threshold for each, however some are slightly different.
- Concern from relatives about the patient’s mental status
- An acute deterioration in the patient’s functional ability (“off legs”)
- Immunosuppressed
- Trauma/Surgery/Procedure in the last 8 weeks
- Respiratory rate between 21 and 24
- Systolic BP between 91-100
- Heart rate between 91-130, or any new abnormal heart rhythm
- Temperature <36°C
- Clinical signs of wound infection
Official Diagnostic Criteria of septic shock
Sepsis
AND
(despite adequate volume resuscitation)
Persistent hypotension, requiring vasopressors to maintain Mean Arterial Pressure (MAP) ≥65 mmHg
AND
Lactate ≥2 mmol/L
Pragmatic approach to diagnosing septic shock
Sepsis
AND
(following fluid resuscitation)
Hypotensive (SBP <90 mmHg)
AND
Lactate >2 mmol/L
Sepsis 6
= BUFALO
BLOOD
IV access
Blood cultures (x2), coag, glucose, lactate, FBC, U&E, CRP
(also culture all other potential sources – e.g. sputum, urine)
URGENT REVIEW
Escalate for senior review (ST3+)
FLUIDS
500 mL crystalloid IV fluid bolus
Catheterise to monitor urine output.
ABX:
High dose broad spectrum IV (BUT remember allergies!)
LACTATE:
Identifies patients at risk
OXYGEN
(if required)
Ongoing care of sepsis patient (post- sepsis 6)
Regular A-E assessment and observations.
Further fluid replacement is guided by lactate and BP.
Thorough clinical examination to find source of infection, if not already obvious.
Consider escalation status
Discuss with Critical Care if:
- Lactate >4 mmol/L or SBP <90 mmHg
- Lactate or SBP remain abnormal despite 20mL/kg fluid bolus, after 1 hour
Neutropaenic Sepsis
= a time-critical and potentially fatal condition occurring in immunocompromised patients.
It is a medical emergency requiring immediate investigation and treatment in hospital.
These patients tend to deteriorate more rapidly
Neutrophil count: < 0.5 × 10^9/L
Risk of sepsis increases with severity (how low) and duration of neutropaenia.
Common causes of neutropaenic sepsis
Systemic Anticancer therapies – chemotherapy/ Radiotherapy
Immunomodulatory therapies
What is important to not miss in patients with neutropaenia?
NEUTROPAENIC SEPSIS
Neutrophil count: < 0.5 × 10^9/L
high index of suspicion, as patients can be APYREXIAL
General Management of an overdose
ABCDE
- Assess GCS, pupil size and reaction to light
- Assess for signs of IVDU
Collateral History
Bloods:
- FBC, U&E, LFT, INR, ABG
- Glucose, paracetamol and salicylate levels
- Further specific assays as guided by national poisons information service.
Reduce absorption:
=> Gastric lavage – rarely used, only within 60 mins of overdose.
=> Activated charcoal
Give antidote, if there is one available
Continue monitoring:
- Plasma levels
- Observations
- Hepatic / renal function
Psychiatric assessment prior to discharge
Use of activated charcoal
Single dose of 50g, in water
Reduces absorption of many drugs – e.g. paracetamol, salicylates
It is not effective for a number of poisonings including: strong acids or bases, iron, lithium, arsenic, methanol, ethanol or ethylene glycol
Antidotes for specific overdoses:
- Paracetamol
- Opiates
- Benzodiazepines
- Beta-blockers
- TCAs
Paracetamol – N-acetylecysteine
Opiates – naloxone
Benzodiazepines – flumazenil
Beta-blockers – atropine, glucagon plus dextrose
TCAs – sodium bicarbonate.
What is a common effect of alcohol intoxication?
Hypoglycaemia is a common effect, as alcohol inhibits gluconeogenesis
More common in children/malnourished adults
NOT responsive to glucagon, so IV glucose is given.
What is the management of alcohol intoxication?
SUPPORTIVE TREATMENT
however:
As blood alcohol levels rise above 400mg/dL, complications may become more severe
=> Respiratory failure, coma, death
If blood alcohol levels rise >500 mg/dL, haemodialysis may be considered.
TCA overdose
Presentation:
- Sinus tachycardia, dilated pupils and urinary retention
- Progresses into drowsiness and coma
Ix:
- ABG – metabolic acidosis
- ECG – widened QRS
Mx:
- Many will recover with supportive Tx only
- IV sodium bicarbonate if SVT/VT
Benzodiazepine overdose
Presentation:
- Drowsiness, ataxia, dysarthria, coma
Management:
- Flumezanil 200 micrograms over 15 seconds
- Further 100 micrograms at 1 minute intervals
- Can induce fits, so monitor for this
Opiate overdose - presentation and Mx
Presentation:
- Respiratory depression, pinpoint pupils, coma
Mx:
- 400 micrograms naloxone IV
- If no response after 1 minute, give a further 800 micrograms
- If still no response at 2 minutes, repeat dose of 800 micrograms
If there is a response, repeat the dose every 2 minutes until breathing is adequate (naloxone has a very short half life).
What is the dose of naloxone used for opiate overdose?
400 micrograms naloxone IV
If no response after 1 minute, give a further 800 micrograms
If still no response at 2 minutes, repeat dose of 800 micrograms
Cocaine overdose - Presentation and Mx
Presentation:
- Agitation, tachycardia, HTN, hyperthermia, sweating, hallucinations
ABG – metabolic acidosis
Mx:
- There is no specific antidote
- IV diazepam for hallucinations/convulsions
- Active external cooling for hyperthermia.
Salicylate overdose
Presentation:
- Vomiting, dehydration, hyperventilation, tinnitus and sweating.
Ix:
- Initially there is respiratory alkalosis due to stimulation of the respiratory centres,
- This develops into a metabolic acidosis.
Get salicylate levels at 2 hours due to continuing absorption:
- If >500 mg/L consider alkalinisation of the urine with sodium bicarbonate and KCl (monitor ECG as this will also increase K+ secretion)
- If >700 mg/L consider dialysis.
GCS - motor response
OUT OF 6
6 – Obeys commands
5 – Localises to pain / any purposeful movement towards stimuli
4 – Withdraws from pain (pulls limb away)
3 – Flexor response to pain (arms flex onto chest)
2 – Extensor response to pain
1 – No response
GCS - verbal response
OUT OF 5
5 – Orientated
4 – Confused conversation (responds to questions, some disorientation)
3 – Inappropriate speech (random speech, no conversational exchange)
2 – Incomprehensible speech (moaning, but no words).
1 – No speech
GCS - eye opening
OUT OF 4
4 – Spontaneous eye opening
3 – Eye opening in response to speech
2 – Eye opening in response to pain
1 – No eye opening
How is GCS measured?
Motor response - out of 6
Verbal response - out of 5
Eye opening - out of 4
Record the best response of any limb and best speech.
The motor response is the best prognostic indicator.
Unconscious patient - differentials
Vascular – stroke, shock, haematoma, SAH
Infective/inflammatory – sepsis, meningitis, encephalitis, abscess.
Trauma – traumatic brain injury
Autoimmune – brainstem demyelination
Metabolic:
- Hypo/hyper – glycaemia, calcaemia, natraemia
- Hypo – adrenalism, thyroidism
- Severe uraemia
- Wernicke-Korsakoff syndrome
Neoplasm – cerebral tumour
Unconscious patient - investigations
Blood and urine tests:
- Routine biochemistry
- Metabolic / endocrine studies
- Drugs screen
- Blood cultures
Imaging:
- Head CT/MRI
Lumbar Puncture:
- If CT excluded mass lesions/raised ICP
Why is the ABO blood group system particularly important to consider when transfusing blood?
the only blood group system in which individuals generate antibodies to antigens absent from their erythrocytes WITHOUT PRIOR EXPOSURE to those antigens.
The formation of the IgM ABO antibodies to antigens absent in an individual begins at birth, but their levels are typically too low for detection until 3-6 months of age
(Other blood group systems require exposure, such as through transfusion of blood products, or in pregnancy).
Rhesus System
comprised of over 50 different antigens, but the most significant is the D antigen (as it is the most immunogenic)
If a rhesus negative individual is exposed to rhesus positive blood products, then they can develop IgG antibodies directed against the rhesus D antigen.
=> If exposed to rhesus positive blood products again, there will be haemolysis.
G&S
For patients undergoing elective surgery where a transfusion is not expected, a “group and save” can be performed, with an antibody screen performed to confirm it is negative.
Then appropriate blood can be made available quickly if required.
If the antibody screen is positive, compatible blood should always be reserved in advance.
Indirect agglutination test
– this test is always performed pre-transfusion
- Donor RBCs added to the patient’s serum, and Coomb’s reagent is added
- Agglutination indicates that the patient serum has antibodies for the donor RBCs
Direct agglutination test
Direct agglutination test – rarely required pre-transfusion
- Patients “washed” RBCs are added to Coomb’s reagent
- If they agglutinate that indicates that there is an autoimmune haemolytic process going on.
- This is also known as “Coomb’s test”
Cross-match - XM
involves physically mixing of patient’s blood with the donor’s blood, in order to see if any immune reaction occurs (agglutination test)
After ensuring that donor blood is compatible, the requested units of donor blood are issued and can be transfused to the patient.
It is not possible for the laboratory to provide crossmatched blood without having processed a G&S sample first.
Which blood products need a cross-match?
all blood products except platelets
Taking G&S or XM samples
Pink bottle
LABEL BOTTLES BY HAND
When requesting blood products:
- Ensure blood sample has been taken
- Consent the patient for transfusion
- Specific form to fill out to request blood.
Important points to mention when consenting a patient for a blood transfusion
- Benefits/indications
- Risks of infection – HIV 3/million, HBV 2/100,000
- Non-infectious risks – transfusion reaction
- Right to refuse – e.g. Jehovahs’ Witness
Major haemorrhage protocol
2 units of O negative blood to be made available immediately
Blood of the same ABO/rhesus group will be available in 10-15 minutes
Fully cross-matched blood will be available in 45 minutes.
Blood products - Packed Red Cells
virtually all plasma removed and replaced by an additive
Used in acute blood loss (surgery, accidents, childbirth), anaemia, haemolytic disease of the newborn, sickle cell disease, etc.
Blood products - Platelet Concentrates
To treat bleeding in severe thrombocytopaenia
Used prophylactically in patients with bone marrow failure to prevent bleeding
Blood products - FFP
Contains all of the coagulation factors present in fresh plasma, so used mainly for replacement of coagulation factors in acquired deficiencies
e.g. liver disease, warfarin overdose (where VitK would be too slow).
Blood products - cryoprecipitate
FFP minus supernatant
Useful in conditions like DIC where the fibrinogen is very low.
Blood products - Factor VIII and IX Concentrates
Specific factor concentrates
Used in haemophilia / vWD
Blood products - albumin
In severe hypoalbuminaemia, where the patient is overloaded and resistant to diuretics.
Blood transfusion - monitoring
Baseline observations – 30-60 mins prior to the start of transfusion
Stay with the patient for the first 5 minutes of the transfusion
=> Observations 15 minutes after the start of the transfusion.
Monitor as appropriate for patient condition for the duration of the transfusion.
=> Every 30 minutes if patient is TACO risk.
Observations at the end of the transfusion.
Monitor for 24 hours after last unit transfused
Transfusion reaction - Acute haemolytic reaction
Suggested by agitation, raised temperature, low BP, abdominal/ chest pain, signs of DIC.
STOP transfusion
A-E resuscitation
Keep IV line patient with 0.9% saline.
Transfusion reaction - Allergy/anaphylaxis
If a simple allergy (urticaria/itch) => slow/stop transfusion and give chlorphenamine with close monitoring.
If anaphylaxis => stop transfusion and treat appropriately
Transfusion reaction - Bacterial contamination
Suggested by rapid onset signs of sepsis and rigors
STOP transfusion
Start sepsis protocol
Send blood unit to the lab along with blood cultures from the patient
Transfusion-related Acute Lung Injury (TRALI)
Basically ARDS due to antibodies in the donor plasma
Suggested by dyspnoea and CXR white out.
Stop the transfusion and treat as ARDS
Non-haemolytic Febrile Transfusion Reaction
Shivering and fever, usually 0.5-1 hour after starting transfusion
Slow the transfusion, administer anti-pyretic and monitor closely.
Mx of Transfusion reaction - fluid overload
Slow or stop transfusion
Give oxygen and diuretic
Consider exchange transfusion
I-MIST-AMBO handover
trauma patient - handover from ambulance crew
Identification
Mechanism of injury
Injuries
Signs
Treatment and trends
Allergies
Medication
Background history
Other information
Trauma Primary Survey
A rapid history should be taken where possible – AMPLE
2 C’s
=> Catastrophic Haemorrhage?
=> C-spine stabilisation?
A to E
AMPLE trauma history
Allergies
Medications
PMH
Last meal
Events leading to accident
A to E in trauma patient
A:
- Jaw thrust only (no head tilt, chin lift) if C-spine in question
- High flow oxygen
B:
- Rate, depth, efficacy
- Feel, look, auscultate, percuss
- Any signs of ATOM FC?
C:
- Pulse, CRT, BP
- Consider “Blood on the floor and 4 more”
D:
- AVPU/GCS
- Glucose
- Check for base of skull/cranial/facial fracture
E:
- Exposure head to toe
- Temperature
ATOM FC
= traumatic chest injuries to look for in a trauma primary survey
- Airway obstruction or disruption
- Tension pneumothorax
- Open pneumothorax
- Massive haemothorax
- Flail chest
- Cardiac tamponade
Trauma - imaging
Seriously ill patient will have a trauma series X-rays in resus:
- C-spine XRs
- CXR
- Pelvic XR
FAST (focussed abdominal sonography for trauma) scans are performed for suspected abdominal injury or bleeding.
=> Can detect organ lacerations / haematomas and free fluid.
CT scanning should only occur once the patient is stable.
Possible traumatic injuries
Pelvic Injuries
Chest Injuries - ATOMFC
Pulmonary Contusion
Aortic Disruption
Myocardial Contusion
Fractures
Dislocations
Trauma - Airway injuries
Indicated by stridor, noisy breathing and s.c. emphysema
Management is as per ATLS:
- Jaw thrust
- Examination/suction
- Temporary airway
- Definitive airway management (intubation)
Open PTX
= Direct communication between the pleural cavity and external environment
Will be obvious on examination, with a “bubbling” wound
Tension PTX can develop
Massive haemothorax - cause and signs
> 1500mL of blood in the pleural cavity.
Most commonly due to rib fracture causing venous injury
Signs are of shock, with lung dull to percussion with no breath sounds.
Massive haemothorax - Mx
Large bore chest drain placed in 6th ICS, mid-clavicular line.
Admit for observation
If there is continuous drainage of >200mL for 4 consecutive hours, the patient should undergo thoracotomy.
Open PTX - Mx
Asherman valve (sterile dressing sealed on 3 sides to create a valve through which air can escape but not enter).
Chest drain (sited away from the wound itself)
Surgical closure.
Flail Chest
Multiple rib fractures, causing a mobile segment
This will characteristically draw in on inspiration.
This is very painful, so much to cause respiratory failure.
Mx:
- These patients require an intercostal block/anaesthesia
- If in respiratory failure or exhausted they may require mechanical ventilation
Cardiac Tamponade - cause and signs
= Bleeding into the pericardial cavity
Prevents ventricular filling, and thus there is a fall in cardiac output.
Usually caused by penetrating trauma
Echo is diagnostic when Beck’s triad is seen on examination:
=> Raised JVP, low BSP, muffled heart sounds
What is Beck’s Triad?
Raised JVP, low SBP, muffled heart sounds
= triad of signs indicating cardiac tamponade
Management of Cardiac Tamponade
Immediate pericardiocentesis to relieve pressure
Thoracotomy as definitive management
Pulmonary Contusion
Blood in the alveolar space, usually due to blunt trauma.
Characterised by worsening hypoxia over 24 hours as the bleeding spreads.
It can be seen as diffuse alveolar shadowing on CXR
Aortic Disruption
Can occur as a result of severe acceleration-deceleration injury.
Presents as per ruptured aortic dissection
Fatal unless false aneurysm develops in the mediastinum.
Myocardial Contusion
Bruising of the myocardium, usually occurs with steering wheel injuries or sternal fractures.
May appear similar to MI on ECG
Tx = conservative
Tetanus prophylaxis for open wounds
Clean, minor wounds – tetanus booster required if uncertain vaccination history, or >10 years since last dose.
All other wounds (including those with any contamination, burns, missile wounds) – give tetanus booster, unless has one in last 5 years.
What features suggest high risk of further suicide post-overdose or suicide-attempt?
Increasing age
Male sex
Living alone
Alcohol/drug abuse
Severe pains states
Severe affective disorder
Recent adverse life events
Active suicidal intent
Actual suicidal intent in the original act:
=> Perceived lethal mechanism
=> Final acts undertaken
=> Made attempts not to be discovered
Suicide attempt - important history points
Was there a clear precipitant for the event?
=> Is that still ongoing or has it resolved?
Was it pre-meditated or impulsive?
=> Is there still continuing suicidal intent?
Did they leave a suicide note?
=> Did they make attempts not to be discovered?
=> What would they do if they went home now?
=> What’s their social support like?
Do they have any psychiatric symptoms – ASSESS MENTAL STATE
Mental state examination
- Appearance and behaviour
- Speech (rate, tone, volume)
- Emotion (mood and affect)
- Perception (hallucinations)
- Thought (formal thought disorder? Delusional content? Suicide/self harm?)
- Insight
- Cognition (orientation to time place and person)
Types of Burn
Thermal
Electrical
Chemical
Radiation
Thermal Burns
Burn due to direct contact with hot object/hot vapour
Depth is determined by:
- temperature,
- duration of exposure,
- relative thickness of the skin
Electrical Burn
Severity depends on strength of voltage and duration of contact.
There is often associated deep tissue damage (blood vessel thrombosis, muscle damage), which can lead to further complications.
Chemical Burn
May penetrate deep into the skin and be difficult to remove, causing continued damage.
Alkali substances tend to cause worse burns.
Radiation Burn
Due to exposure to radiation
(such as sunburn caused by UV radiation)
Associated with cancer due to DNA damage
How is the severity of a burn determined?
- The depth,
=> Generally divided into full or partial thickness burns - The amount of skin involved,
- Associated clinical features.
Partial thickness burns
Epithelial elements are spared in partial thickness burns, which eventually allows spontaneous healing
suggested by:
- erythema that blanches on pressure,
- retains sterile pinprick sensation
- bleeds on irritation
Can be further classified as:
1. superficial erythema,
2. superficial partial thickness
3. deep partial thickness burns
Burns - Superficial Erythema
A superficial burn that leads to blanching erythema due to capillary dilation, with or without blistering produced by plasma exudation.
The underlying germinal layer is intact, and the skin will heal in a few days.
Burns - Superficial Partial Thickness
The burn extends down through the epidermis to involve the germinal layer, but the dermal appendages such as the sweat glands and hair follicles remain largely preserved.
There is intense blistering and sloughing of the skin, which separates after about 10 days to leave healed skin.
Burns - Deep Partial Thickness
The burn extends to the germinal layer and destroys a significant proportion of the dermis and appendages.
Healing is much slower, and associated with scarring.
Burns - Full Thickness
= Complete destruction of the skin and germinal layer, with any initial blistering quickly replaced by slough, which separates only slowly over 3-4 weeks to leave an underlying surface of granulation tissue.
Clinically:
- Non-blanching
- Do not bleed on needle testing
- Sensation is absent.
Full thickness burn - healing
If very small, they may heal from ingrowing epithelium from adjacent tissue, but most often they heal by dense scar tissue with consequent contracture and deformity unless grafted.
Measuring the size of a Burn
Lund and Browder chart => allows accurate estimation of burn surface area.
In adults, the “rule of 9’s” is often used to estimate body surface area involved:
- 9% head and neck, and each arm.
- 18% each leg, front of the trunk, back of the trunk
- 1% = the perineum
Another useful alternative is to use the patient’s palm and fingers to represent 1% of the body surface area. This is useful for estimating the surface area of small burns.
Burns - systemic features
AIRWAY :
Smoke inhalation or direct thermal injury can rapidly result in laryngeal/pharyngeal oedema and airway obstruction
HYPOVOLAEMIC SHOCK
- severe loss of plasma, particularly in the first 24 hours.
- This amount of loss is proportional to the area of the burn rather than its depth and leads to intravascular depletion and shock.
ANAEMIA:
- Occurs due to destruction of red cells in involved capillaries
PAIN:
- More severe in superficial burns
- Deep burns may be relatively painless due to extensive destruction of nerve endings.
Signs of airway involvement in a burns patient
History of fire in enclosed space
Signs of stridor
Tachypnoea / dyspnoea
Singed nasal hair
Facial burns
Harsh cough
Carbonaceous sputum
Securing the airway should always be a priority if this is suspected, with senior anaesthetic review required.
Management of burns patients
Immediate First Aid:
- Stop the burning process straight away
- Remove overlying clothing (may contain heat) and apply cool running water to the area.
- Cling film can be used temporarily
Resuscitation:
- If the burn area is over 15% (10% in a child), admit for IV fluids.
Assessment of Burn severity:
- In terms of depth, extent and location of burn.
Subsequent Tx:
- Manage the local condition, mitigate systemic effects, then focus on reconstruction and rehabilitation.
Systemic Management of burns
Pain will require IV opiates.
Fluid replacement is essential
Catheterise to ensure adequate urine output.
Systemic ABX are only required if there is evidence of invasive infection.
Nutrition should be managed carefully, with parenteral nutrition required early if enteral nutrition is not possible.
Fluid replacement in burns
Volume of Hartmann’s in the first 24 hours required calculated according to the Parkland formula.
4 mL x Total burn surface area x weight (kg)
Half of this should be given in the 1st 8 hours
The other half should be given in hours 8-24 (from the time of the burn)
Partial Thickness Burns - local management
Simple, non-adherent dressings (e.g. paraffin-impregnated gauze) used, with a topical antibiotic if infection is suspected.
If the hands are involved, they may be covered in sulfadiazine cream and placed in a sealed polythene bag.
Full Thickness Burns - local management
Total excision of the burn wound is required
Smaller defects can be closed primarily
Larger defects require skin grafting (this may be required for some deep partial thickness burns also).
When are there special considerations in management of burns?
FULL THICKNESS BURNS
=> can constrict to restrict the blood slow to limbs, or restrict breathing in the chest
=> must be incised acutely with an escharotomy
BURNS ON THE HANDS
=> scarring can result in contractures and significant disability
=> they should be splinted in the position of function, elevated, and early burn excision and grafting may be indicated.
Early complications of burns
Wound sepsis – invariably due to S. pyogenes in the 1st week, or Pseudomonas thereafter.
Wound contractures in circumferential burns
Late complications of burns
Sepsis – from the wound and also inhalation-related chest infection
Acute peptic ulceration = Curling’s ulcer
AKI – due to hypovolaemia and precipitation of haemo/myoglobin
Psychological disturbances
Burn - skin grafting
Should be performed within 5 days of the burn, although wounds must be free of infection.
Best = autograft split skin from unburnt areas
When should a patient with burns be managed in a specialist burns centre?
Burns >30% of total body area (TBA)
Partial thickness burns >10% (or 5% in children)
Full thickness burns >1%
Circumferential injury
Associated inhalation injury
Chemical or electrical injuries
Extremes of age.
Which burns patients are suitable for outpatient management?
Adults with partial thickness burns <10%
Children with partial thickness burns <5%
Full thickness burns <1%
= reassurance and analgesia; blisters need to be deroofed and dressed with paraffin gauze.
Patients will be referred to a burns centre if not healed by 3 weeks (assumed full thickness)
What are possible causes of epistaxis ?
What are predisposing factors?
Causes:
- Idiopathic or Nose-picking = most common
- Trauma
- Infection
- Tumours
Predisposing factors:
- HTN
- Anticoagulants, NSAIDs, aspirin
- Coagulopathies
- Hereditary Haemorrhagic Telangiectasia
Epistaxis - features suggesting posterior bleed
Profuse
Bilateral
Failed anterior packing
What is the source of most cases of Epistaxis?
90% occurs from Little’s area (anterior bleed)
Epistaxis - Management
- First aid
* Lean forward, pinch fleshy part – for 10 mins
* Apply ice to bridge of nose
* Avoid swallowing blood - Resuscitation (if severe)
* A to E – estimate blood loss, measure pulse/BP
* FBC, coag screen, G&S
* IV fluids if needed - Cauterisation:
* If bleeding from Little’s area (i.e. anterior bleed)
* Using silver nitrate or bipolar diathermy - Packing:
* If cannot visualise or cauterise bleed
* Need prophylactic ABX
* First line – anterior packing
* Second line – posterior packing - Sphenopalatine artery ligation
- Surgery – if cannot stop bleed
Earache
Ear pain can be referred from many other structures.
In children, if there is a preceding URTI, suspect acute otitis media.
acute otitis media - presentation and management
Sx = hearing loss, pain, otorrhoea (when the TM bursts), pyrexia and systemic upset.
Signs = red, bulging TM
1st line Mx = amoxicillin, but myringotomy may be required if it fails to resolve or if there are neurological sequelae
Always examine to r/o the possibility of mastoiditis
=> Other complications – facial nerve palsy, labyrinthitis, intracranial infections.
Corneal foreign body - Mx
Apply topical anaesthetic to the eye
Use a fluorescein drop at the slit lamp to stain abrasions and enhance visualisation of foreign bodies
Evert the eyelid with cotton bud
If the foreign body is embedded in the cornea, get senior help
Ocular Pain - differentials
Discomfort:
- Conjunctivitis, thyroid eye disease, dry eye, blepharitis
Pain on eye movement
- Optic neuritis (other Sx = loss of vision over days, especially colour vision
Pain around the eye
- GCA, orbital cellulitis
Severe pain:
- Anterior uveitis
- Bacterial keratitis
- Acute angle-closure glaucoma
- Scleritis/episcleritis
Optic neuritis - presentation
Pain on eye movement
other Sx = loss of vision over days, especially colour vision
Anterior uveitis - presentation and Mx
PAIN + also photophobia, blurred vision, red eye, synechiae
Tx = topical steroids, mydriatics, ABX
Bacterial Keratitis - presentation and Mx
Pain and blurred vision, hypopyon
Tx = topical ABX
Acute angle-closure glaucoma - presentation and Mx
Also red eye, blurred vision, photophobia, headache, nausea
EMERGENCY – treat with IV acetazolamide, topical pilocarpine every 5 mins, and topical beta-blockers initially
Scleritis/episcleritis - presentation and Mx
PAIN and also red eye, intense pain and blurred vision with scleritis
Tenderness with episcleritis
Tx = topical NSAIDs for episcleritis, systemic steroids for scleritis.
Causes of sudden vision loss
PAINFUL
Angle closure glaucoma
Uveitis
Optic neuritis
GCA
PAINLESS
Ischaemic optic neuropathy
Retinal artery occlusion
Retinal vein occlusion
Retinal detachment (previous floaters/flashing lights)
Age-related macular degeneration
Vitreous haemorrhage
Intracranial disease affecting visual pathway
What is general anaesthetic?
How is this typically done?
= a state of total unconsciousness, resulting from the use of centrally-acting drugs
Patients are pre-oxygenated and usually have IV induction before gas maintenance with volatile agents
Anaesthesia - IV induction agents
propofol
thiopentone
Anaesthesia - Volatile agents
isoflurane
halothane
Anaesthesia - Inhalation induction
e.g. in needle-phobics or in those where difficult intubation is expected.
Inhalation induction maintains spontaneous respiration
Total IV anaesthesia (TIVA) - indications
Should be used in patients with PMH or FH of malignant hyperthermia (volatile agents are contraindicated in such patients)
Other advantages of TIVA:
- Reduced PONV
- Predictability in bariatric patients
- More control over depth of anaesthesia
Rapid Sequence Induction (RSI)
the delivery of a rapidly acting muscle relaxant immediately after the induction agent, without waiting to see if respiration can be assisted with a bag-mask system.
This then runs the risk of being unable to intubate/ventilate an unconscious paient, and thus “difficult airway” equipment should always be available.
It is used to rapidly produce optimum conditions for intubation in the emergency situation (e.g. non-starved trauma patients).
The triad of GA
Narcosis – patient rendered unconscious
Analgesia – lack of pain and suppression of physiological reflexes.
Relaxation – reduction / absence of muscle tone, using muscle relaxants.
Local Anaesthesia
Blockage of conduction of nerve impulses along nerve axons by injection of lignocaine, usually alongside adrenaline to vasoconstrict.
Vasoconstriction increases the potency and duration of anaesthesia.
Can be used topically (e.g. prior to cannulation in children) or by local infiltration or minor procedures (e.g. suturing).
Regional Anaesthesia
Local anaesthetic injected directly into:
a) minor nerves (e.g ulnar / intercostal blockade)
b) major nerves (e.g. brachial plexus)
c) the epidural space or CSF
General benefits = less risk of chest infections, CV complications, PONV, post-op pain and DVT.
Spinal Anaesthesia
LA solutions introduced via a needle directly into the CSF, producing spinal anaesthesia.
Onset is fast, and lasts 1-4 hours.
There is a complete sensory block in the affected area
=> Loss of pain, temperature and positional sense.
Monitoring in spinal anaesthesia
The patient should be continuously monitored with ECG, BP, RR, SpO2.
=> Sympathetic blockade can lead to hypotension, so vasoconstrictors and fluids may be required.
Contraindications to spinal anaesthesia
Raised ICP,
Hypovolaemia,
Surgery above the thorax,
Local/systemic infection
Procedures lasting >2 hours.
Epidural Anaesthesia
Epidural catheter inserted into epidural space, then LA (plus analgesics) can be delivered continuously via a pump.
Can take up to 45 minutes for surgical anaesthesia to be achieved (slower onset than spinal)
Level of anaesthesia then depends on the amount of anaesthetic used.
Epidural anaesthesia - Indications
May be used in longer O&G or orthopaedic surgery
On-demand system for pain relief (e.g. labour or post-op).
Epidural Anaesthesia - Monitoring
The patient should be continuously monitored with ECG, BP, RR and SpO2
Complications = hypotension, respiratory depression, CSF/dural puncture (giving a headache and total spinal effect).
Effects of CV/respiratory disease on anaesthesia
pre-existing CV disease => risk of peri-operative myocardial ischaemia and MI
pre-existing respiratory disease => risk of post-op complications
Thorough pre-op assessment is required
+/- ECG, Echo, CXR, ABG, pulmonary function
Effects of GA on body systems
CV:
- Decreased myocardial contractility, thus decreased CO and hypotension
- Arrythmias can develop.
RESP:
- Respiratory depression can occur, alongside decreased ventilatory responses to hypoxia/hypercapnia.
- Laryngospasm leading to airway obstruction can also occur.
Effects of spinal anaesthesia on body systems
CV:
- Blockage of sympathetic nerves can lead to vasodilation and bradycardia.
RESP:
- If opiates are being used, respiratory depression can occur.
GA - main risks
Post-op nausea / vomiting (PONV)
Anaphylaxis
Awareness under GA
Aspiration
=> Use RSI if patient not starved
Cardio-respiratory issues.
Spinal - main risks
Neurological disorder due to trauma
High spinal block – depression of brainstem
Urinary retention and bladder damage – catheterise to avoid this
Cardio-respiratory issues
Spinal headaches
PONV if opiates used.
ASA 1
= Normal, healthy patient
e.g. Healthy, non-smoking, no or minimal alcohol use
ASA 2
= Patient with mild systemic disease
e.g. Current smoker, social alcohol drinker, pregnancy, obesity (30<BMI<40), well-controlled DM/HTN, mild lung disease
ASA 3
= Patient with severe systemic disease, restricting activity but not incapacitating.
e.g. One or more moderate to severe diseases. Poorly controlled DM or HTN, COPD, morbid obesity (BMI ≥40), active hepatitis, alcohol dependence or abuse, implanted pacemaker, moderate reduction of ejection fraction, ESRD undergoing regularly scheduled dialysis, history (>3 months) of MI, CVA, TIA, or CAD/stents
ASA 4
= Patient with severe systemic disease, representing a constant threat to life.
e.g. Recent (<3 months) MI, CVA, TIA or CAD/stents, ongoing cardiac ischemia or severe valve dysfunction, severe reduction of ejection fraction, shock, sepsis, DIC, ARD or ESRD not undergoing regularly scheduled dialysis
ASA 5
= Moribund patient, not expected to survive 24 hours without operation
e.g. Ruptured abdominal/thoracic aneurysm, massive trauma, intracranial bleed with mass effect, ischaemic bowel in the face of significant cardiac pathology or multiple organ/system dysfunction
ASA 6
= Declared brain-dead patient, whose organs are being harvested for donor purposes.
Operative urgency
IMMEDIATE = to save life or limb
- Resuscitation and surgery simultaneous
- Patient should be in theatre within minutes.
URGENT = acute onset / deterioration of a condition threatening life, limb or organ.
- Surgery takes place once resuscitation complete (within 6-24 hours).
EXPEDITED = stable patient requiring early intervention.
- Within days of decision to operate.
ELECTIVE = surgery planned and booked in advance of admission to hospital.
Pre-op anaesthetic assessment
generally based on thorough history and examination
Other investigations are based on findings
Pre-op anaesthetic assessment investigations
U&Es
- Important if on digoxin/diuretics/steroids
- Also patients with DM, renal disease, vomiting/diarrhoea.
LFTs:
- If known hepatic disease, Hx of alcoholism, metastatic disease or malnutrition.
Blood glucose:
- DM or long-term steroids.
Clotting:
- If Hx or FHx of bleeding or on anticoagulation
CXR
- If Hx of cardiorespiratory disease, or suspected/known malignancy.
Echo:
- To assess LVF in patients with ischaemic or valvular disease, that have exercise ability limited by another condition.
Respiratory function tests:
- In those with dyspnoea, COPD or asthma.
C-spine XR
- In RA patients, Hx of major trauma, or difficult intubation.
Starvation times pre-op
The aim is to minimise the volume of gastric contents, thus lowering the risk of regurgitation and aspiration.
Solid food (including milk) = 6 hours
Breastfed infants = 4 hours
Clear fluids (including black tea/coffee) = 2 hours
Minimise starvation time => increased pre-op starvation leads to greater dehydration, PONV, anxiety and discomfort.
Diabetic patient - pre-op
Minimise pre-op fasting times – ideally first on the operating list.
Comprehensive pre-op assessment and investigations
If DM well controlled with diet/tablets, medication should be omitted on the day of surgery.
If they are poorly controlled or on insulin, Pt will need VRIII.
Diabetic patient - peri-op
Consider RSI, as diabetic patients are prone to aspiration.
Regular monitoring of blood glucose levels.
If blood glucose >10 mmol/L, consider an insulin/glucose regimen.
Diabetic patient - post-op
Regular monitoring of blood sugar and vital signs
PONV - pathophysiology
Involves input to the vomiting centre from:
- Higher cortical centres – memory/fear
- The stomach/small intestine – direct surgical effects
- The chemoreceptor trigger – anaesthetic drugs and opioids.
PONV - RFs
Patient:
=> F>M, non-smoker, previous Hx of PONV
Procedure:
=> Abdominal, gynae or ENT
Anaesthetic:
=> Longer duration of surgery, GA, use of inhalation agents.
Post-op:
=> pain, opioid analgesia, dehydration, hypotension
PONV treatment pathway
Cyclizine – 50 mg/8h IV/IM/PO
Prochlorperazine – 12.5mg / 6h IM
Ondansetron – 4mg/8h PO/IV
Dexamethasone 8mg IV can be added at any stage if nausea is not controlled
Cyclizine
Antihistamine
Useful antiemetic in middle ear surgery and motion sickness
CI – heart failure, BPH, hepatic/renal disease
Metoclopramide / Prochlorperazine / Domperidone
Dopamine agonists – stabilise the CTZ and have prokinetic effects
Metoclopramide is relatively ineffective in PONV
CI – prochlorperazine is CI’d in Parkinson’s
Ondansetron
= Most effective in PONV
5-HT3 antagonist
Effective in the prevention of PONV by blocking vagal afferents from the gut/CTZ
Can be given prophylactically
Caution in : Hepatic impairment, QT prolongation, pregnancy/breastfeeding.
Dexamethasone as an anti-emetic
Glucocorticoid with unknown MOA acting to augment the effects of other anti-emetics.
Should be used early on in treatment pathway.
Post-op oxygen therapy
Anaesthetic agents exert a dose-dependent depression on the sensitivity of central chemoreceptors, reducing the stimulatory effect of CO2.
=> Supplementary oxygen may be needed for at least 72 hours.
Patients who chronically retain CO2 (advanced COPD) should be titrated using a venturi mask to prevent hypoventilation and monitored by serial ABG
Different venturi masks
Blue – 24% inspired oxygen, 1-4 L/min
White – 28% inspired oxygen, 4-6 L/min
Yellow – 35% inspired oxygen, 8-10 L/min
Red – 40% inspired oxygen, 10-12 L/min
Green – 60% inspired oxygen, 12-15 L/min
How much oxygen can a nasal cannula deliver?
2-4 L/min, plus room air
Limitations of pulse oximetry in monitoring oxygenation
Cannot distinguish between CO and O2
Does not reflect the oxygen carrying capacity of the blood
=> E.g. in anaemia, hypovolaemia
In hypovolaemic patients, it may not be able to get a reading.
Anything that leads to venous pulsation can cause the probe to read the venous rather than arterial saturations
=> E.g. tricuspid regurgitation or occluded venous return (when the probe is taped on very tightly).
Can be affected by nail polish.
Pre-op - patients taking warfarin
Stop 7-10 days before surgery (AT LEAST 5 DAYS)
On the day, if INR <1.5, surgery can go ahead.
If patient is high risk, can be substituted with LWMH (shorter acting), which is then withheld the evening before surgery.
Pre-op - patients taking Clopidogrel
Stop 7 days before surgery
Pre-op - patients taking COCP
Should ideally be stopped 4 weeks before major operations
Restarted at the first menses that occurs at least 2 weeks after mobilisation.
Switching to the POP is acceptable.
“Blood on the floor and 4 more”
1) active haemorrhage outside the body
2) in the thigh compartments of bilateral femur fractures
3) pelvis
4) abdomen
5) chest
