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).
