Acutely Unwell Flashcards
Obstructive airway risks:
hypoxic injury to the brain, heart, kidneys and can lead to cardiac arrest and death
Partial airway obstruction - 3x added sounds and indications
Snoring - indicates a loss of tone
Gargling - indicates fluid such as secretion, blood or vomit
Stridor (inspiratory wheeze) indicates larynx obstruction
Signs of complete airway obstruction
Silent see saw movement of the chest
A paradoxical movement of abdomen and chest as the body tries to force oxygen past the obstruction
What is imminent with see saw chest?
Cardiac arrest
Most common cause of airway obstruction:
reduced / loss of consciousness
This causes a loss of soft tissue tone in the upper airway most notably the soft palate
Causes a snoring sound
3 further causes of airway obstruction (not LOC)
Foregin body - food, vomit, or blood
Oedema - Infection, Burn, Anaphylaxis
Tumor or abscess
Most common cause of airway obstruction in childre
foreign body
When to avoid head tilt chin lift manoeuvre
suspected head or neck trauma
Which airway is used in conscious patient?
Nasopharyngeal
When is nasopharyngeal airway contraindicated
Basal skull fracture - insertion -> risk of epistaxis
Signs of basal skull fracture
CSF rhinorrhea is a sign of this Battle sign (bruising over mastoid process from posterior auricular artery) and racoon eyes are signs of this
They are only for use in deeply unconscious patients as they can cause gag
Oropharyngeal airway
How to measure oropharyngeal airway
from mandibular angle to incisor.
3 things to look for to assess breathing
Colour of the patient - are they cyanosed
Resp rate - is this normal?
O2 sats and if they’re on supplemental oxygen
3 things to feel for to assess breathing
Tracheal deviation - this is uncomfortable and not the most reliable
Chest wall movements - equal and full
Percuss anterior and posterior
3 things to listen for to assess breathing
Equal air entry
Added sounds
Reduced sound
O2 sats target (usual) and type of O2
Get sats to targets of 94-98 using high flow oxygen via a non rebreather mask
O2 sats target t2rf
Target in patients of hypercapnic resp failure (COPD) is 88-92
Hypoxia kills before hypercapnia so aim for 94-98 unless 100% they are a retainer
Other steps to take action for breathing
Request ABG (pre and post oxygen) and CXR
Re asses and move on
Are their sats coming up?
2 things to look for to assess circulation
Colour of the patient centrally and peripherally
Do they look dehydrated or sweaty
5 things to feel for/measure to assess circulation
Temperature - central and peripheral
Pulse - peripheral and centrally, weak peripheral pulse - hypotension. Bounding pulse - early sepsis sign.
Capillary refill time >2 seconds is abnormal
Blood pressure
JVP
Listen for to assess circulation
Heart sounds for arrhythmias
3 potential areas which can cause hypotension and causes
Heart - arrhythmias, ACS and acute LVF
Pipes - sepsis and anaphylaxis giving systemic vasodilation
Fluid - hypovolemia from dehydration of haemorrhage
4 steps to manage acute haemorhhage
Stop the bleeding
Apply pressure
Contact a surgeon
Give packed red cells as crystalloid can’t carry oxygen
3 parts of disability
Conscious level _ AVPU
Pupil size and reactivity
Glucose - abcDEFG - don’t ever forget glucose
How to assess consciousness
AVPU Alert and talking Responds to verbal stimulus Responds to Painful stimulus (supraorbital pressure) Unresponsive
Pupils findings
Pinpoint - think opiate OD - Naloxone
Uneven response - IC event so urgent CT head
Blood glucose below 4
Administer 100ml 20% dextrose IV
Steps for reduced consciousness
Anyway with reduced conscious level is at risk of obstruction
Place in left lateral position
Protect airway with a GCS below 8
Anaphylaxis definition
a severe systemic hypersensitivity reaction characterized by rapidly developing life threatening airway/breathing/circulation problems as well as skin/mucosal changes.
However 20% of patients have no redness, rash or swelling
Biphasic anaphylaxis
is a recurrence of symptoms within 72 hours of full recovery without any additional exposure to the allergen. The faster they respond to initial treatment the less likely this is
Suspected anaphylaxis
is the term used to describe patients presenting to the ED with anaphylactic-like symptoms and it is treated as anaphylaxis but is not diagnosed as this until the patient has seen a specialist allergist.
5 common triggers of anaphylaxis
Food most common - nuts and shellfish Insect venom Latex - this is common in healthcare workers or patients who are in the hosp alot having lots of procedures Idiopathic Drugs
5 common drug triggers of anaphylaxis
Antibiotics
Anesthetic
Contrast
NSAID - cox 1 inhibition causing mast cell independent angioedema and bronchospasm
Vancomycin - calcium phosphate mechanism of non allergic mast cell activation
3 ways in which anaphylaxis is triggered
Immunologically mediated (allergic), Non immunological (non allergic), Idiopathic
Anaphylaxis pathophys. allergic
Sensitization (clinically silent):
first exposure -> mature B cells to produce IgE antibodies -> bind to mast cells and basophil receptors
2nd exposure:
Allergen cross links to the IgE receptors -> mast cells to degranulate -> releases preformed (histamine and tryptase) and newly formed (prostaglandin D2, leukotrienes and thromboxane )
Resulting in anaphylaxis
Mast cell activated anaphylaxis pathophys
Direct non specific activation of histamine releasing agent
Calcium phospholipase mechanism seen in vancomycin and red man syndrome
Mastocytosis
MRGPRX2 model NMBA which is yet to be proven in humans
Mast cell independent anaphylaxis pathophys
Cox 1 inhibition causing bronchospasm and or angioedema
NSAID
The Big 3 criteria of anaphylaxis
- Sudden onset and rapid progression of symptoms
- Life threatening ABC symptoms
- Skin and mucosal changes - red, rashy and puffy
Only 80% have these changes
Adrenaline is dosed on weight in children but a good framework is
Above 12 - adult dose = 500 micrograms
6-12 - 0.3mg at 1 in 1000 = 300micograms
<6 - 0.15mg at 1 in 1000 = 150 micrograms
5 steps to Managing anaphylaxis
A-E IM Adrenaline per dose IV fluid bolus challenge: Adult 500ml to 1L, Child at 20ml/kg Chlorpheniramine hydrocortisone
Define Bacteraemia -
viable bacteria in the blood
Define sepsis
a life threatening organ dysfunction due to a dysregulated host immune response to infection. The patient will die without treatment
Define septic shock
This is when the arterial blood pressure drops resulting in hypoperfusion of organs despite fluid resus. This will lead to a high lactate as the organs enter anaerobic respiration. This can be measured with either a BP or <90 systolic despite fluid resus or lactate above 4.
Define multiple organ dysfunction syndrome
- severe septic shock and organ failure beyond possible recovery.
Pathophysiology vasodilation in sepsis
Macrophage, lymphocytes and mast cells identify the pathogen and They release cytokines such as interleukins and TNF to active immune system
The cytokines activate further immune system cells which eventually lead to NO being released - vasodilation throughout the body
Pathophysiology oedema in sepsis
Many cytokines cause endothelial lining permeability to increase meaning that fluids leak into the extracellular space and oedema as well as a reduction in IV volume. The oedema creates a space between blood and tissue so less oxygen reaches the tissue.
Inflammatory response also leads to pulmonary edema bibasal crackles can be heard which means people often think a pneumonia is causing the sepsis when in reality it could be an infection from elsewhere
Pathophysiology coagulation in sepsis
The coagulation system is activated and fibrin is deposited throughout the systemic circulation compromising perfusion more. It also consumes platelets and clotting factors as they are being used up. This will lead to a thrombocytopenia and hemorrhage with an inability to form clots to stop them. This is known as disseminated intravascular coagulation
Lactate raised in sepsis because…
this is raised due to tissue hypoperfusion which switches the tissues into anaerobic - of which lactate is a product
Hypotension and tachycardia is caused in sepsis by
the drop in systemic vascular resistance meaning the heart has to pump more to maintain cardiac output
Infections predisposing to sepsis
35% Pneumonia - strep pneumoniae 25% UTI E.Coli - most common in over 65’s 11% Abdominal infection gram neg Ruptured viscus Anastomotic leak Pancreatitis, peritonitis and appendicitis 11% Skin, soft tissue - staph aureus Endocarditis Device related Meningitis or encephalitis
6 rf for sepsis
Extremes of age meaning under 1 and over 75
Chronic conditions such as COPD and diabetes
Chemotherapy, immunosuppression steroids
Surgery, recent trauma or burns
Pregnancy or peripartum
Any indwelling medical device such as a catheter or central line
8 signs of sepsis on examination
Any sign of potential source of infection eg chest infection (cough), cellulitis, wound discharge or dysuria
Reduced urine output
Cyanosis
Non blanching rash - meningococcal septicaemia
New onset AF or arrhythmia
Warm skin due to dilation
Long septic shock will be cold as SNS over powers - bad sign
Short cap refill and bounding pulse
4 key things to be aware of in sepsis
Tachypnoea is often a first sign of sepsis
Elderly patients often present with confusion or drowsiness
Neutropenic / immunosuppressed patients may have normal obs but be life threatening il
N+V and hyperglycaemia can also occur in septic patients
8 sepsis red flags
Altered mental state RR above 35 Systolic BP below 90 or 20% lower than normal O2 sats below 94 or needing 40l oxygen to maintain it Lactate above 2 Coagulopathy and rash HR above 130 Recent chemo within 2-3 weeks
Sepsis 6
Lactate
Serial lactates
Good for seeing if they response to treatment
High - bad prognosis
Blood culture
Urine output - can respond to cardiac output faster than BP. minum 0.5ml/kg/Hr
Oxygen
Broad spec AB
Every 1 hour delay increases mortality by 7.6%
Fluid
500ml crystalloid in 15 mins
If severe hypotension or lactate above 2 they get fluid at 30ml/kg stat so a 75kg man gets 2.25 litres over an hour
Septic shock management
Treat with aggressive IV fluids. If IV fluid bolus does not increase their BP and lactate then they should be educated to ICU where they can be started on Inotropes such as noradrenaline.
Neutropenic sepsis
This is a medical emergency. It is sepsis in a person with a neutrophil count of less than 1x10 to the power of 9. Low neutrophils are usually the consequence of anticancer or immunosuppressants.
5 Clinical features of acute haemorrhage
Pallor
Cool peripheries
Clammy skin
Hypotensive and tachycardic
Be aware young patients may not be because they have vascular tone to compensate
Some old patients may be on drugs to stop the physiology eg beta blockers would stop a tachycardia
3 things to look for (when stable) in acute haemorrhage
Check for bleeding in rectum, vagina and PR and any other places
Check abdomen for things like cullens and grey turner’s sign
Cullens is umbilical discolouration to intra abdominal bleed of any kind
Grey turners is along the flanks often associated with hemorrhagic pancreatitis
Assess long bones and the pelvis
5 areas prone to heavy bleeds
skull, chest, abdomen, pelvis and retroperitoneum
Classification of bleeding
- Physiology is normal but are bleeding (<15% blood loss)
- Slight changes in physiology but remain normotensive however slightly tachy (30%)
- Becoming hypotensive and v tach. On edge of severe haemorrhage. (40%)
- Severe hypo and tacchy. (>40% = dead)
Major haemorrhage is defined as
a 50% blood loss in 3 hours or >150ml per minute. That works out to 2500 ml in a 70kg male. Normal circulating blood volume is 65/70ml/kg.
Which 3 areas are found on CT polytauma
intrathoracic, abdominal and cranial trauma
What is the lethal triad of bleeding
Hypothermia, acidosis, coagulopathy
Why is hypothermia a major problem in haemorrhage
impairs platelet and enzymatic function within the clotting cascade
Why is acidosis a major problem in haemorrhage
tissue hypoperfusion leads to lactic acidosis which impairs clotting
What 4 steps should be taken with hypothermia in haemorrhage
Limit exposure, remove wet clothing and ensure good temperature
Continually monitor temperature via rectal probe
Use warming blankets forced air if available
Rapid transfusion of warmed blood products
What 2 steps should be taken with acidosis in haemorrhage
Restore perfusion ASAP with haemostatic resuscitation ignoring traditional 1-2L of crystalloid
Maximise oxygenation and minimise hypoventilation to remove any potential for additional respiratory acidosis
What should be avoided in acidosis with haemorrhage and why
Worsened by administration of crystalloid due to a delusional anaemia effect
What 3 steps should be taken with coagulopathy in haemorrhage
Liaise with haematology from the outset as initial clotting screen is inaccurate in acute haemorrhage
Manage major haemorrhage patients as if they are coagulopathic don’t wait for lab results
Thromboelastography can provide good information if available
Which 4 things are part of damage control resuscitation is done to prevent the lethal triad occurring in haemorrhage
haemostatic resuscitation, permissive hypotension and early damage control surgery
Permissive hypotension is…
the act of maintaining a blood pressure lower than physiologic levels in a patient that has suffered from hemorrhagic blood loss.
A compromise between ensuring adequate tissue perfusion and reducing the risk of delusional coagulopathy and clot disruption
5 features of Managing hemorrhage
Oxygen 15/L reservoir 2 wide bore cannula peripheral access Bloods - FBC, Us and Es, Liver screen, CLotting screen and group and save CT angiography Warmed fluid/blood products
what reverses dabigatran
Idaruciamab
4 ways to reverse warfarin and timings
stop warfarin
vitamin K (4-24h)
Fresh frozen plasma (less common now)
Human prothrombin complex (<1 hour but under 6h half life so give vit K also)
Reversing warfarin in emergency major bleed - 3 steps
Stop warfarin
Give phytomenadione which is a vitamin K1 slow IV
Give prothrombin complex - factor 2,7,9 and 10
Reversing warfarin with Inr above 8 and a minor bleed (3 steps)
Stop warfarin
Give phytomenadione which is a vitamin K1 slow IV
Give prothrombin complex - factor 2,7,9 and 10
Reversing warfarin with Inr above 8 no bleed
Give phytomenadione by mouth
Reversing warfarin with Inr 5-8 minor bleed
Phyomenadione slow IV
Reversing warfarin with Inr 5-8 no bleed
Withhold 1-2 dose of warfarin and reduce maintenance at lower dose
When is warfarin restarted
INR < 5
