Acute Care Flashcards
What is shock?
= a life-threatening failure of oxygen delivery to tissues.
It is a pathophysiological state, which has a number of underlying causes
What is the triad of signs associated with shock?
- Signs of reduced perfusion
• Prolonged capillary refill time
• Reduced urine output
• Altered mental state. - Low blood pressure
- Raised lactate.
Why is lactate raised in a patient with shock?
Anaerobic respiration produces lactate, which accumulates in the blood, causing a hyperlactataemia
End diastolic volume and End Systolic volume
EDV depends on how well the heart is able to fill.
=> Preload
=> Compliance – stretchiness/relaxation of the heart.
ESV depends on how well the heart is able to empty.
=> Contractility – force of contraction
=> Afterload
What are the four broad types of shock?
- Hypovolaemic
- Distributive
- Cardiogenic
- Obstructive
Effect of sympathetic stimulation on heart rate
Increases HR
Effect of parasympathetic stimulation on heart rate
Decreases HR
When does hypovolaemic shock occur?
What are the results of this?
when there is insufficient volume of blood in the intravascular compartment (i.e. a problem with Preload).
Reduces End-Diastolic Volume
Which reduces Stroke Volume
Which reduces Cardiac Output
Which causes low Blood Pressure
Compensation of hypovolaemic shock
Increase in Systemic Vascular Resistance due to peripheral vasoconstriction => Appear peripherally “shut down”
Vasoconstriction limited to least critical organs – skin, gut, kidneys.
Perfusion of vital organs (heart, lungs, brain) maintained.
Increase in Heart Rate => Tachycardia
Signs and Symptoms of hypovolaemic shock
General shock symptoms and signs.
Signs of hypovolaemia/dehydration
Peripheral shut down – cool peripheries, mottled skin
What are the “general” signs of shock?
↓BP,
↓Urine output,
↑CRT
Altered mental state
What are signs of hypovolaemia/dehydration
Sunken eyes, dry mouth, thirst
When does Distributive Shock occur?
when there is failure of vasoregulation (i.e. a problem with the systemic vascular resistance)
This may be due to:
• Loss of sympathetic tone
• Widespread vasodilatation due to toxins
A huge drop in vascular resistance directly causes a drop in blood pressure
Compensation of distributive shock
Tachycardia
May have increased contractility/compliance
Signs and symptoms of distributive shock
General shock symptoms and signs.
Signs of abnormal vasodilatation
=> Flushed complexion, warm peripheries (in contrast with every other category of shock).
When does cardiogenic shock occur?
What can cause this?
Occurs when the heart stops pumping effectively. This may be due to:
- Reduced contractility
- Reduced compliance
- Bradycardia – reduce the cardiac output
- Tachycardia / arrhythmia – prevent the ventricles from filling properly.
Compensation of cardiogenic shock
Will depend on the specific cause – increase in HR/contractility depending on which isn’t affected.
Increase in systemic vascular resistance due to peripheral vasoconstriction
Signs and symptoms of cariogenic shock
General shock symptoms and signs.
Peripheral shut down.
Fluid status may be normal (often overloaded in patients with heart failure)
When does obstructive shock occur?
Occurs when there is blockage of blood flow, either in a great vessel or of the heart itself.
Blockages can affect:
- Preload – vena cava/pulmonary circulation (e.g. compression due to mediastinal shift in tension PTX or massive PE).
- Afterload – aorta (e.g. aortic dissection)
- Compliance – cardiac (e.g. cardiac tamponade)
Compensation of obstructive shock
Increase in systemic vascular resistance due to peripheral vasoconstriction
Tachycardia
Signs and symptoms of obstructive shock
General shock symptoms and signs.
Peripheral shut down
Fluid status may be normal
=> Check neck veins for distension, which may indicate obstruction, rather than fluid overload
Which type of shock will cause a different peripheral temperature?
Distributive shock will cause warm peripheries, whereas other types will cause cool peripheries.
Haemorrhagic shock
= a subtype of hypovolaemic shock
There is a relationship between the volume of blood loss and the signs and symptoms that are observed.
The different classes of haemorrhagic shock allow you to estimate volume of blood loss based on signs and symptoms.
It is important to manage the cause as well as replacing blood/fluid.
Anaphylactic shock
A mixed picture of shock.
- Widespread histamine release has a profound vasodilatory effect which causes a distributive shock.
- Histamine also increases the permeability of the vessels, leading to excessive loss of fluid into the interstitial space (“third-space losses”) – hypovolaemic shock.
How to manage anaphylactic shock
Remove the trigger
Administer adrenaline and antihistamines.
Fluid boluses to correct hypovolaemia
(Steroids?)
How does adrenaline help in managing anaphylactic shock?
acts on adrenergic receptors in the sympathetic nervous system to reverse the systemic vasodilation, acting as a vasopressor.
it also decreases vessel permeability, which helps to prevent further third-space fluid losses.
Steroids in managing anaphylaxis
usually hydrocortisone
likely to reduce the likelihood of a biphasic anaphylaxis (i.e. a second event), rather than having any role in correcting the current abnormalities.
Septic Shock
A mixed picture – Bacterial endotoxins have an effect of:
- Widespread vasodilatation (causing distributive shock)
- Increasing vessel permeability (causing hypovolaemia through third-space losses).
Management of septic shock
Remove trigger - urgent antibiotics
Fluid boluses to correct hypovolaemia
In cases refractory to fluid boluses, referral to HDU or ITU for infusion of vasopressors
Neurogenic shock
occurs when there is an injury to the central nervous system above the T6 level
=> total loss of sympathetic tone whilst leaving vagal stimulation unopposed.
profound vasodilatation causing a distributive shock, but potentially with no tachycardia as compensation due to the loss of sympathetic stimulation
What should be considered in a case of distributive shock with paradoxical bradycardia
neurogenic shock - ?injury to the brain or spinal cord
Management of neurogenic shock
Any/all of:
- Fluid resuscitation
- Vasopressors to reverse systemic vasodilatation
- Inotropes to increase myocardial contractility
- Chronotropes to correct the Bradycardia
Prolonged supportive measures during recovery (~1-3 weeks)
Examples of vasopressors
vasopressin (ADH), adrenaline, noradrenaline, etc
Examples of inotropes
dopamine, isoprenaline, adrenaline, noradrenaline, etc
Examples of chronotropes
atropine, adrenaline, dopamine, etc.
Effects of shock on the heart
Increased HR may lead to myocardial ischaemia, though coronary perfusion is preferentially maintained
Effects of shock on the kidney
pre-renal AKI due to reduced perfusion
Effects of shock on the brain
Cerebral perfusion is maintained for as long as possible
Depending on degree and duration of shock - can get hypoxic brain injury
Effects of shock on the lungs
reduced perfusion can cause Type 1 respiratory failure acutely, even after resuscitation
Effects of shock on the gut
Reduced perfusion can cause mucosal ischaemia - may lead to stress ulceration over time
Initial monitoring in shock
A-E assessment (and regular reassessment)
Obs repeated regularly
Hourly Urine Output monitoring – Insert urinary catheter
Blood gas - for lactate, and for acid-base/respiratory status
Bloods
ECG
Monitoring in severe/refractory cases of shock
Admission to HDU (Level 2)/ITU (Level 3)
Advanced monitoring:
- Central Venous Pressure monitoring via Central Venous Catheter (CVC/Central Line)
- Invasive Blood Pressure monitoring via Arterial Line (A-Line)
- Continuous cardiac monitoring
Management of Shock
High-flow (15L) oxygen via a non-rebreathe mask
Establish IV access early
IV fluid resuscitation (unless obvious Cardiogenic shock)
Treat the Cause
- Vasopressors (if SVR impaired)
- Inotropes (if Contractility impaired)
- Chronotropes (if HR impaired)
- Cardioversion (if arrhythmias present) – chemical or DC
Don’t forget to reassess and escalate if needed.
When is DKA considered severe?
What should be done?
Ketones >6 pH <7.1 HCO3 <5 / anion gap >16 K+ <3.5 GCS <12 SpO2 <92% SBP <90 Pulse >100 or <60
HDU/ITU must be contacted
Why is potassium monitoring important in DKA?
Potassium levels can fluctuate severely during DKA
=> osmotic diuresis (due to glucosuria) leads to a total body K+ (and phosphate) depletion.
=> Life threatening hypokalaemia can occur with insulin infusion.
BUT Serum potassium levels may not mirror this and may be low/normal/high.
So continuous monitoring of potassium is essential and replacement may be required.
when is cardiac monitoring required with a K+ infusion?
if rate >20 mmol/hour
Management of HHS
- IV Fluid replacement – to replace loss caused by the hyperglycaemia
- IV insulin – to bring the blood glucose level down.
=> but often very sensitive to insulin and require much lower doses than in DKA.
= > Aim is to reduce glucose levels slowly. - Treat any underlying cause, if known
- Refer to diabetes specialist nurse – education for prevention of further emergencies.
What is considered hypoglycaemia?
glucose <4.0 mmol/L
What are some causes of hypoglycaemia?
Delayed/missed meals
Low carbohydrate content in meals
Unplanned or strenuous exercise
Taking too much insulin
What are some symptoms of hypoglycaemia?
Fatigue, Sweating, Pallor, Headache Tachycardia
Management of hypoglycaemia - conscious patient who is able to swallow
If conscious and able to swallow:
- 15–20 g of fast-acting carbohydrate
- Repeat treatment after 10–15 minutes, up to a maximum of 3 treatments in total.
- Once glucose >4mmol/L, long-acting carbohydrate should be given to prevent blood glucose from falling again.
Management of hypoglycaemia - if unconscious/unable to swallow/seizures
- Glucagon or glucose 10% (or 20%) infusion.
- Long-acting carbohydrate should be given as soon as possible.
(Patients who have received glucagon require a larger portion of long-acting carbohydrate to replenish glycogen stores)
What is self harm?
self-poisoning or self-injury, irrespective of the apparent purpose of the act.
=> it’s not an illness itself but is more or less dangerous behaviour that should alert us to an underlying problem, difficulty or disorder.
What is suicide?
= an intentional self-inflicted act that results in death
Suicide - epidemiology
~10 deaths per 100,000 in the UK
1/3rd of all suicides in the UK are men in their 40s and 50s
~90% are suffering from a psychiatric disorder at the time of death
Risk factors for self harm
F:M = 1.5 : 1
Increased incidence in some ethnic groups
Previous self-harm (40% of people who present have a history of self-harm)
Diagnosis of personality disorder
Alcohol / drug misuse
Lower socioeconomic status, social isolation
Hopelessness, impulsivity, poor problem-solving ability
Sexual abuse, traumatic life events
Recent significant life events
Risk factors for suicide
Statement of intent and access to means
Psychiatric illness – depressive illness, early schizophrenia, comorbidity, recent discharge from hospital
History of previous self-harm,
History of violence
Family history of self-harm and suicide
Social isolation, unemployed, lower social class, single, Significant life events e.g. bereavement
Painful physical illness
Impulsive personality traits
Male
Older age
Factors associated with HIGH Risk:
- Recurrent and persistent suicidal ideation,
- Hopelessness, Agitation, Intoxication,
- Delusions of control, poverty, guilt,
- Impulsive personality traits, poor engagement with services
Suicide in post-partum period
women presenting in the post-partum period.
Deaths in post-partum period are more likely to be by violent means
Postpartum psychosis is associated with 70x risk
Assessment of self harm/suicide
History
Assessment of Mental State
Management of self harm/suicide
involves a Bio-psychosocial approach to minimise risk to self and others
is discharge safe or is admission needed?
What is sepsis?
a life-threatening organ dysfunction due to a dysregulated host response to infection
what is septic shock?
= a subset of sepsis where particularly profound circulatory, cellular and metabolic abnormalities substantially increase mortality
Recognising sepsis
Previously, the SIRS criteria were used (with sepsis being SIRS + evidence of infection)
Now, NEWS2 scores are used
NEWS2 score of 5+ should trigger a sepsis screen if one of the risk factors is present, or if a HCP is concerned.
Risk factors for recognising sepsis
- 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)
Also some more specific risk factors in pregnancy and neonates.
What infections are the most common causes of sepsis?
- Pneumonia
- UTI
- Abdominal infection
- Skin, soft tissue, bone/joint infections
- Other infections – endocarditis, device-related, meningitis, etc.
What things count for “suspicion of infection” ?
Suggestive diagnostic results
Clinical suspicion
Signs of infection – e.g. fever, high/low temperature, sweating, flushing; but with no suggestion of source.
How is sepsis diagnosed?
SOFA Score - the “Official” diagnostic criterion for diagnosis of organ dysfunction (and therefore Sepsis)
Can only really be used in critical care situations
Therefore, “red flag” sepsis criteria used more frequently
RED FLAG SEPSIS
- 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 saturations of 92% or above (or 88% in COPD)
- 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
If any one of these is present, START SEPSIS SIX.
AMBER SEPSIS
mostly match up with the red flag criteria, with a lower threshold for each
- 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
If any one of these are present, FURTHER REVIEW REQUIRED.
Diagnosis of septic shock
Sepsis AND (following fluid resuscitation) Hypotensive (SBP <90 mmHg) AND Lactate >2 mmol/L
As a trigger to call Critical Care
Initial management of Sepsis
BUFALO:
Blood – IV access – cultures, coag, glucose, lactate FBC, U&E, CRP
(culture all other potential sources – e.g. sputum, urine)
Urgent Review – escalate for senior review (ST3+)
Fluids – fluid bolus of 500ml and monitor urine output.
Antibiotics – high dose broad spectrum BUT remember allergies!
Lactate – identifies patients at risk
Oxygen – give if required (aim for 94-98% or 88-92% in hypercapnic failure)
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 than those without neutropaenia.
Diagnosis of neutropenic sepsis
= Neutrophil count: < 0.5 × 10^9/L
The risk of sepsis increases with severity (how low) and duration of neutropaenia.
Maintain a high level of suspicion
Management of neutropenic sepsis
- Rapid A-E assessment
- Escalation onto Sepsis 6 pathway
=> CRITICAL: Commence antibiotics within 1 hour - Treat on suspicion - DO NOT DELAY whilst awaiting confirmation of neutropaenia via bloods
- Consider potential for atypical infections
What are the concerns in an apyrexial patient with neutropaenia?
further deterioration is often experienced before they are recognised as being septic.
Signs and symptoms of an overdose
Depends on the substance in question, quantities ingested and the timeline of presentation.
Often there are no signs or symptoms early on.
Paracetamol overdose - signs and symptoms
nausea and vomiting,
Loin pain/haematuria – renal failure
RUQ pain/jaundice – hepatic necrosis
benzodiazepine overdose - signs and symptoms
CNS depression, ataxia, slurred speech, respiratory depression
opioid overdose - signs and symptoms
respiratory depression, pin-point pupils, coma
alcohol intoxication - signs and symptoms
dependent on the amount of alcohol consumed (i.e. dose dependent)
- Euphoria, social disinhibition, joyousness
- Extraversion, decreased reasoning
- Ataxia, nausea and vomiting
- Anterograde amnesia
- CNS depression
Investigations in overdose
- Observations
- Physical examination (especially neurological)
- ABG/VBG
- ECG
- Baseline bloods (especially renal and hepatic function)
- Serum levels of substance in question
Why are symptoms of alcohol dose dependent?
Alcohol is metabolised through zero-order metabolism – the rate of reaction is independent of concentration.
The enzymes become saturated, so the body can’t keep pace with the rising concentration
Management of alcohol intoxication
If needed, treatment is supportive – e.g. recovery position, monitoring vital signs, sometimes IV fluids.
Alcohol withdrawal
seen in alcohol dependent states (usually >20 units/day)
typical symptoms include sweating, tremor, anxiety, nausea and vomiting.
More serious symptoms:
- Confusion,
- Hallucinations
- Very high temperature
- Seizures
Delirium tremens
= rapid onset of confusion usually caused by withdrawal from alcohol
What hallucinations in particular tend to be associated with alcohol withdrawal?
formication (a type of tactile hallucination) – the feeling of imaginary insects/spiders on the skin.
Management of alcohol withdrawal
Medically assisted withdrawal is the treatment of choice.
Benzodiazepine (e.g. chlordiazepoxide) + Pabrinex (vitamins B&C)
Either symptom-triggered or fixed-dose reducing regimen
what causes acute Wernicke’s Encephalopathy?
Exhaustion of vitamin B1 (thiamine) leads to biochemical lesions in the CNS.
what can cause vitamin B deficiency in alcoholics?
Often diet deficient in thiamine, but also alcohol prevents absorption of thiamine.
how does Wernicke’s Encephalopathy present?
Typically present with a triad of:
- Ataxia
- Ophthalmoplegia
- Confusion (new onset)
Treatment of Wernicke’s Encephalopathy?
high-dose parenteral thiamine (e.g. Pabrinex) often leads to full resolution of symptoms, if given quickly.
IV or IM
Korsakoff’s Syndrome
= Irreversible brain damage, typically due to chronic alcohol misuse.
Often there have been previous instances of acute Wernicke’s encephalopathy.
Typically presents with dense anterograde amnesia, confabulation and personality change.
- Often have similar needs to someone with dementia.
- Can believe made up things with a delusional intensity.
Investigations in paracetamol overdose
Serum paracetamol levels
=> Only valid after 4 hours post-ingestion.
Baseline bloods to assess renal and liver function (includes INR)
ABG/VBG to assess acid/base status
Weight - will guide treatment later on
Treatment of paracetamol overdose
Patients on/above the treatment line for paracetamol overdose will be treated with acetylcysteine.
If overdose is staggered, paracetamol levels are difficult to interpret – treat with acetylcysteine
Acetylcysteine is given in a 21-hour infusion, based on the weight of the patient.
Psychiatric assessment after patient is stable.
What does haematemesis indicate?
Vomiting of bright red blood indicates an acute upper GI bleed
DDx for haematemesis
Peptic Ulcer Disease
Variceal Bleeding
Oesophagitis
Mallory-weiss tear
Upper GI malignancy
Rare causes (<5%) - aorta-enteric fistula, AV malformation, etc.
Coffee-ground vomit
Vomiting of black material
= blood altered by gastric acid
Melaena
Black, tarry stools = blood digested by intestinal enzymes.
Usually upper GI bleed, but can be small bowel or right side of colon.
Haematochezia
Fresh, red blood per rectum.
= Usually colonic/rectal bleeding
Sometimes profuse upper GI bleeding, which stimulates peristalsis and results in rapid transit of blood (~10% of haematochezia)
Management of GI bleed
A-E assessment
=> may be pale, tachycardia, hypotensive
Abdominal exam
PR exam
Bloods - FBC, U&E, LFT, coag, XM, VBG
Imaging - OGD, (CT contrast), (erect CXR)
What is the Glasgow-Blatchford Bleeding score?
Callculated pre-endoscopy.
Evaluating the likelihood of need for intervention.
Scores range from 0 – 23,
=> Score = 0 – patient may be suitable for outpatient care.
=> Score >0 – consider admission for endoscopy
=> Score = 6+ – indicates 50% chance of intervention being required (transfusion/OGD/surgery)
What is the Rockall score?
Used to predict the risk of re-bleeding and death.
Requires both pre- and post-endoscopy findings.
If the total Rockall score is 3+, this indicates a significant risk of re-bleeding.
At what point in the GI tract is a bleed considered to be “lower GI”?
blood loss occurring from a site distal to the ligament of Treitz (duodenal-jejunal junction).
PR bleeding - occult blood
No visible blood
Iron deficiency anaemia
+ve FOB or FIT
PR bleeding - moderate bleeding
Rectal bleeding or melaena
Haemodynamically stable
PR bleeding - severe bleeding
Large amounts of rectal bleeding
Postural hypotension +/- Significant drop in haematocrit
Haemodynamically unstable
Persistent bleeding/rebleeding
Requires multiple blood transfusions
DDx for PR bleeding
Haemorrhoids Anal fissure IBD Colorectal cancer Diverticular disease Angiodysplasia UGI bleed Haemorrhagic infective gastroenteritis
Angiodysplasia
Acquired submucosal AV malformations
Most commonly located in caecum and ascending colon.
Most commonly presents with iron deficiency anaemia and occult bleeding
Typical presentation is of painless, fresh, PR bleed in elderly patients
Can be difficult to differentiate from diverticular bleeding.
Investigations for PR bleeding
A-E assessment if severe
Abdominal exam
PR exam
Stool cultures
Faecal calprotectin
Bloods - FBC, U&E, LFT, coagulation, G&S, XM, ferritin/iron studies, VBG
Why are tall people more likely to be affected by PTX?
the gradient of negative pleural pressure increases from the lung base to the apex
=> alveoli at the lung apex in tall individuals are subject to significantly greater distending pressure than those at the base of the lung
predispose to the development of apical subpleural blebs.
How does a primary spontaneous PTX occur?
No underlying lung disease
Rupture of a pleural bleb
How does a secondary spontaneous PTX occur?
Due to underlying lung disease:
COPD, asthma, severe pulmonary fibrosis, etc.
Who are most likely to get primary/secondary spontaneous PTXs?
Primary - young, tall (and thin?) males.
Secondary - older patients (>40), usually smokers
Difference in clinical signs between primary and secondary PTX?
Primary - symptoms can be minimal - low index of suspicion is required.
Secondary - symptoms more likely to be severe, even with a small PTX
PTX - symptoms
Sudden onset pleuritic chest pain
Potentially pallor and tachycardia (tension???)
If small, potentially no symptoms.
PTX - signs on affected side
Reduced chest expansion
Hyper-resonance on percussion
Diminished breath sounds on auscultation
What are signs of a TENSION PTX?
Trachial deviation (away from affected side) Cyanosis Severe tachypnoea Tachycardia Hypotension
how does tension PTX occur?
one-way valve system at the site of the breach in the pleural membrane
allows air to enter the pleural cavity during inspiration but preventing release of air during expiration.
This increases the intrapleural pressure so that it exceeds atmospheric pressure.
This results in impaired venous return and reduced cardiac output results in the typical features of hypoxaemia and haemodynamic compromise.
Who is tension PTX most likely to affect?
Ventilated patients on ITU Trauma patients Resuscitated patients (CPR) Lung disease: acute asthma or COPD Blocked or clamped chest drains Patients on non-invasive ventilation Hyperbaric oxygen treatment (very small patient group)
Management of tension PTX
- call for help immediately.
- Oxygen therapy
- Needle decompression with a cannula
=> 2nd intercostal space, midclavicular line with a 14g (orange) cannula.
=> If initial treatment at 2nd ICS fails, then try 4th/5th ICS. - After decompression, patient will require rapid insertion of a chest drain.
Size of PTX
The general rule is that a 2cm interpleural distance at the level of the hilum equates to a pneumothorax of 50% of the volume of the lung.
<2cm is a small pneumothorax and patient may not need treatment
What are fluids commonly prescribed for?
- Fluid resuscitation
- Fluid maintenance
- Fluid replacement
Fluid compartments of the body
intracellular (ICF) and extracellular (ECF).
ECF
=> interstitial compartment
=> intravascular compartment
How much of the body’s water is in the ICF and ECF?
~65% in ICF
~35% in ECF
=> 75% is interstitial
=> 25% is intravascular
Starling’s hypothesis of fluid movement
fluid movement due to filtration across the wall of a capillary is dependent on the balance between the hydrostatic pressure gradient and the oncotic pressure gradient across the capillary.
solute concentrations of ICF
high potassium concentration.
low sodium concentration.
Intracellular solute concentrations remain more or less constant
solute concentrations of ECF
high sodium concentration.
low potassium concentration.
what determines oncotic pressure gradient?
large molecular weight particles such as proteins in the intravascular compartment create a pressure gradient drawing water towards it.
what determines oncotic pressure gradient ?
affected by circulatory pressures and other pressures in tissues such as oedema, and mechanical restriction such as with infection, plaster casts or bandaging.
What are sources of fluid for the body?
- Oral fluids.
- Parenteral fluids.
- Water released from metabolism (about 400 ml per day, but not normally included in fluid balance calculations).
What are sources of fluid loss?
Urine
GI losses
Insensible losses (skin/breathing/etc).
Others - e.g. drains, burns, bleeding.
How much fluid is lost in the urine per day?
Depends, but usually ~1.5-2L
aim for a minimum urine output of 0.5mL/kg/day
How much fluid is lost from the GI tract per day?
Normally minor (approximately 100 ml/day lost via the faeces)
Can be substantial in someone with diarrhoea, vomiting, biliary drains and high stoma output.
How much fluid is lost from insensible losses per day?
500 – 800 ml per day
can increase significantly (e.g. if patient is sweating, febrile, tachypnoeic, or undergoing open cavity surgery).
what is the maintenance fluid requirement in an average healthy adult, with no extra losses?
2 - 2.5L
what is the ideal combination for maintenance fluids?
25-30 ml/kg/day of water
Approximately 1 mmol/kg/day each of sodium, chloride and potassium
50 - 100 g/day of glucose to limit starvation ketosis
when would you consider prescribing LESS maintenance fluids ?
older adults and/or frail,
renal/cardiac failure,
malnourished and at risk of refeeding syndrome
What are the typical electrolyte requirements for an average healthy adult requiring intravenous fluid for routine maintenance ?
Sodium 1 mmol/kg/day
Chloride 1 mmol/kg/day
Potassium 1 mmol/kg/day
What electrolytes are lost during sweating?
Sodium
What electrolytes are lost through diarrhoea/increased stoma output?
sodium, potassium and bicarbonate
What electrolytes are lost through vomiting?
potassium, chloride and hydrogen ions
What electrolytes are lost through insensible losses?
none - essentially pure water loss
what are the two major classes of fluid for parenteral administration?
- Crystalloids - solutions of mineral salts.
2. Colloids - contain larger water-insoluble molecules such as complex branched carbohydrates or gelatins
Crystalloids
Cheap and effective solutions.
Do not cause adverse immunological reactions.
Can be used as maintenance and replacement fluid.
Depending on their solute concentration, they are classified as hypo-, hyper- or isotonic solutions.
What is an example of an isotonic fluid and how will this redistribute?
e.g. sodium chloride 0.9%
stays almost entirely within the extracellular compartment
What is an example of a hypertonic fluid and how will this redistribute?
e.g. sodium chloride 3%, mannitol
increase plasma tonicity and draw fluid out of cells
What is an example of a hypotonic fluid and how will this redistribute?
e.g. sodium chloride 0.45%
lower serum osmolarity and are not commonly used
despite redistribution, why can crystalloids still be used for fluid resuscitation?
initially when they are rapidly infused, they do cause a transient expansion of the plasma volume.
In emergency - do not wait till the ideal fluid becomes available, give whatever is available to maintain haemodynamic stability.
How will a litre of sodium chloride 0.9% redistribute after administration?
isotonic - stays in ECF
25% to intravascular (250ml)
75% to interstitial (750ml)
Colloids
include: Blood, Dextrans, Gelatin (e.g. gelofusine), Human albumin solution, Hydroxyethyl starch (HES)
exert an osmotic force across the capillary membrane drawing fluid in from the interstitial to the intravascular compartment
- Higher cost.
- Small, but well-established risk of anaphylactoid reactions and anaphylaxis
What does NICE guidance suggest for fluid resuscitation?
500 ml of a crystalloid containing sodium in the range 130-154 mmol/litre (e.g. sodium chloride 0.9%) administered over less than 15 minutes.
Human albumin solution 4-5% can be considered for fluid resuscitation only in patients with severe sepsis
Why should human albumin solution 20% not be used for fluid resuscitation?
it is hyperoncotic => rapid administration can lead to rapid volume expansion and cardiac failure
What should be reviewed/monitored during fluid resuscitation?
mean arterial pressure,
urine output
other clinical measures (e.g. capillary refill).
what does the passive leg raise manoeuvre do?
mimics the administration of a fluid bolus by redirecting blood from the lower limbs to the heart (i.e. increased pre-load)
Used to predict which patients are most likely to respond to administration of a fluid bolus
What are complications of fluid overload?
- Dilutional hyponatraemia
2. Pulmonary oedema
What are some ways of managing fluid overload?
Stop IV fluids
Restrict oral fluids
Furosemide
Nitrates - reduce preload
what is assessed in an A-E assessment ?
A - Airway B - Breathing C - Circulation D - Disability E - Exposure
AIRWAY assessment
Can the patient talk?
If no:
Look for signs of airway compromise – e.g. cyanosis, see-saw breathing, use of accessory muscles, diminished/added breath sounds.
Open the mouth and inspect – ?obstruction with secretions/foreign object.
Any added noises – snoring, crowing, gurgling, stridor.
What are some causes of airway compromise?
Inhaled foreign body
Blood/vomit/secretions in the airway
Soft tissue swelling
Local mass effect
Laryngospasm
Depressed level of consciousness
AIRWAY management
Seek immediate support from anaesthetist and crash team.
Airway manoeuvres:
=> Head tilt chin lift
=> Jaw thrust
Airway adjuncts:
=> Oro/nasopharyngeal airway
BREATHING assessment
Is the patient speaking in full sentences?
Is the patient orientated or confused?
Respiratory Rate
=> Normal (12-20)/ bradypnoea/ tachypnoea
O2 Sats
=> 94-98% in healthy individuals
=> 88-92% in patients with COPD
Tracheal position – any deviation?
Chest expansion – symmetrical? any reduced movement?
Percussion and Auscultation
ABG
CXR
BREATHING management
Position of patient.
Continuous saturation monitoring.
Oxygen therapy (+ nebuliser therapy?)
CIRCULATION assessment
Pulse
=> Rate – Normal/bradycardia/tachycardia?
=> Rhythm, character and volume
MANUAL Blood Pressure
=> Normal/hypotension/hypertension
Obvious signs of dehydration?
Pallor?
Oedema?
Measure capillary refill time (may need to assess central CRT)
=> Should be <2 seconds.
Auscultate Heart Sounds
CIRCULATION problems
- Sepsis
- Dehydration
- Blood loss
- Drugs
- Electrolyte abnormalities
- Ischaemia
- MI
CIRCULATION management
IV access with cannula
FBC, U&Es, LFTs routinely, and consider additional bloods (lactate, ABG, etc).
12-lead ECG if appropriate.
Hypovolaemia requires IV fluid resuscitation to avoid cardiac arrest.
DISABILITY assessment
Assess consciousness - AVPU
(if a more detailed assessment is required, then GCS)
Pupils
=> Inspect the size and symmetry of the patient’s pupils
=> Assess direct and consensual light reflex.
Drug chart review
=> Any drugs which may alter consciousness? (e.g. opioids, sedatives, etc).
Blood glucose
=> Normal 4.0 – 11.0 mmol/L
=> If elevated, check ketones (?DKA)
CT head if intracranial pathology suspected
AVPU scale
Alert: the patient is fully alert, although not necessarily orientated.
(New) Confusion
Verbal: the patient makes some kind of response when you talk to them (e.g. words, grunt).
Pain: the patient responds to a painful stimulus (e.g. supraorbital pressure).
Unresponsive: the patient does not show evidence of any eye, voice or motor responses to pain.
What are the 3 categories in GCS?
Eye Opening
Verbal Response
Motor Response
GCS - eye opening
Spontaneous – E4 To sound – E3 To pressure – E2 None – E1 (NT)
GCS - verbal response
Orientated – V5 Confused – V4 Words – V3 Sounds – V2 None – V1 (NT)
GCS - motor response
Obey commands – M6 Localising – M5 Normal flexion – M4 Abnormal flexion – M3 Extension – M2 None – M1 (NT)
DISABILITY management
Maintain airway if GCS 8 or below.
Naloxone if ?opioid toxicity.
Management of DKA/HHS or Hypoglycaemia.
EXPOSURE assessment
Head-to-toe examination of the patient, front and back. Aim to maintain dignity and control temperature.
Skin
=> Rashes, bruising, signs of infection?
IV lines
=> Redness/discharge?
Abdominal distension
Calves
=> Erythema, swelling, tenderness?
Surgical wounds
=> Signs of infection?
Evidence of haemorrhage
Evidence of infection
Review output from catheter/drains
Review body temperature.
