Emergency Conditions Flashcards
What is anaphylaxis
A life threatening medical emergency caused by a severe type 1 hypersensitivity reaction
Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals, which is known as mast cell degranulation
This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise (which is the key diffentiation factor from a non-anaphylactic allergic reaction)
How does anaphylaxis present
History of exposure to an allergen
Rapid onset of allergic symptoms:
-Urticaria
-Itching
-Angiodema (swelling round lips and eyes)
-Abdominal pain
Additional symptoms:
-SOB
-Wheeze
-Swelling of the larynx, causing stridor
-Tachycardia
-Lightheadedness
-Collapse
How is anaphylaxis managed
Immediate medical attention and management
A to E:
-A - secure the airway
-B - provide o2, salbutamol and ipratropium bromide for wheezing
-C - provide IV bolus of fluids
-D - lie the patient flat to improve cerebral perfusion
-E - look for flushing, urticaria and angio-oedema, remove trigger
Once anaphylaxis diagnosed give:
-IM adrenaline, 1:1000 as per age related guidelines, repeated after 5 mins if required, if no improvement after 2 doses, give IM every 5 mins until adequate response, IV only given in secondary care
-Antihistamines, eg oral chlorphenamine or cetirizine
-Steroids, usually IV hydrocortisone
After:
-Observation - risk of biphasic reactions meaning a second anaphylactic reaction after successful treatment of the first
-Confirm by measuring the serum mast cell tryptase within 6 hours of the event
-Education and follow up with family trained in BLS and specialist referral and training in use of adrenalin auto injector
What are the indications for an adrenalin auto injector
Epipen, Jext and Emerade are trade names for adrenalin auto injector devices
Given to all children and adolescents with anaphylactic reactions and considered in those with generalised allergic reactions (without anaphylaxis) with risk factors:
-Asthma requiring steroids
-Poor access to medical treatment (eg rural)
-Adolescents, who are higher risk
-Nut ot insect sting allergies are higher risk
-Significant co-morbidities eg cardiac disease
How is an adrenalin autoinjector used
Confirm diagnosis of anaphylaxis
Prepare device by removing the safety cap on the non-needle end
Grip the device ina fist with needle pointing down
Administer injection by firmly jabbing the device into outer portion of the mid thigh until device clicks.
Can be done through clothing
Time to hold depends on brand (epipen 3 secs, jext 10 secs)
Remove the device and gently massage area for 10 secs
Phone emergency
Second dose may be given with new pen after 5 mins if required
What is sepsis
A condition where the body launches a large immune response to an infection that causes systemic inflammation and affects the functioning of the organs of the body
What is the pathophysiology of sepsis
Bacteria or other pathogens recognised by macrophages, lymphocytes and mast cells. These cells release vast amounts of cytokines like interleukins and tumor necrosis factor to alert the immune system of an invader. These cytokines activate other parts of the immune system
The immune activation leads to further release of chemical such as nitrous oxide that causes vasodilation. This immune response causes inflammation throughout the body
Cytokine cause endothelial lining of blood vessels to become more permeable, causing fluid to leak out of the blood and in to the extracellular space leading to oedema and a reduction in intravascular volume with the oedema around the vessels increasing space between the blood and tissues, reducing oxygen perfusion of tissues
Activation of the coagulation system leads to fibrin deposition throughout the circulation further compromising organ and tissue perfusion and leads to consumption of platelets and clotting factors as they are used up to form the clots within the circulator system. This leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is known as disseminated intravascular coagulopathy (DIC)
Blood lactate rises due to hypoperfusion of tissues that starves the tissues of o2 causing the switch to anaerobic respiration, a waste product of that being lactate.
What is septic shick
When arterial blood pressure drops and results in organ hypoperfusion, leading to a rise in blood lactate as the organs begin anaerobic respiration.
Measured as either:
-systolic BP <90 despite fluid resuscitation
-Hyperlactaemia (lactate >4mmol/L)
How is septic shock treated
Aggressively with IV fluids to improve the BP and tissue perfusion
If IV fluid boluses don’t improve BP and lactate level then they need to escalate to HDU or ICU where they can use inotropes (eg noradrenalin) to stimulate the CV system and improve bp and tissue perfusion
What is severe sepsis
When sepsis is present and results in organ dysfunction:
-hypoxia
-oliguria
-AKI
-thrombocytopenia
-coagulation dysfunction
-hypotension
-hyperlactaemia (>2mmol/l)
What are the risk factors for sepsis
Any condition that impacts the immune system or makes the patient more frail or prone to infection is a risk factor:
-very young or old (<1 or >75 y/o)
-chronic conditions eg copd and diabetes
-chemo, immunosuppressants or steroids
-surgery or recent trauma or burns
-pregnancy or peripartum
-indwelling medical devices eg catheters or central lines
How does sepsis present
NEWS to catch signs
-temp
-HR
-RR
-O2 sats
-BP
-Consciousness level
O/E:
-signs of potential sources eg cellulitis, discharge from a wound, cough or dysuria
-non-blanching rash can indicate meningococcal septicaemia
-Reduced urine output
-Mottled skin
-Cyanosis
-Arrhythmias eg new AF
High RR (tachypnoea) often first sign of sepsis)
Elderly often present wtih confusion or drowsiness or simply “off legs”
Neutropenic or immunosuppressed patients may have normal obs and temp despite being life threateningly unwell
How is sepsis investigated
Arrange blood tests for patients with suspected sepsis:
-Full blood count to assess cell count including white cells and neutrophils
-U&Es to assess kidney function and for acute kidney injury
-LFTs to assess liver function and for possible source of infection
-CRP to assess inflammation
-Clotting to assess for disseminated intravascular coagulopathy (DIC)
-Blood cultures to assess for bacteraemia
-Blood gas to assess lactate, pH and glucose
Additional investigations can be helpful in locating the source of the infection:
-Urine dipstick and culture
-Chest xray
-CT scan if intra-abdominal infection or abscess is suspected
-Lumbar puncture for meningitis or encephalitis
How is sepsis managed
Hospital’s sepsis protocol
Assess and treat within 1 hour of presentation with suspected sepsis
Perform sepsis six (three tests and three treatments)
Escalate to senior and appropriate care level eg HDU or ICU if needed
Sepsis six:
-blood lactate
-blood cultures
-urine output
-O2 to maintain sats at 94-98% (or 88-92% in retainers)
-Empirical broad spectrum antibiotics
-IV fluids
What is neutropenic sepsis
Medical emergency
Sepsis in a patient with a low neutrophil count of less than 1 x10^9/L
Usually consequence of anti-cancer or immunosuppressant treatment
Treat any temp >38C in these patients as neut sepsis until proven otherwise
At high risk of death from sepsis as their immune system cannot fight the infection well enough
Need emergency admission and careful management
Treat with immediate broad spectrum antibiotics eg tazocin and other management is same as in sepsis but with extra precaution. Treat before results back, don’t wait!
What is shock
An abnormality of the circulatory system that results from reduced organ perfusion and tissue oxygenation
What are the causes of shock
Reduced cardiac output:
-Hypovolaemic shock
– Haemorrhage
— external
— internal
– Vomiting
– Diarrhoea
– Diuresis
– Burns
-Cardiogenic shock:
– MI
– Myocardial contusion
– Myocarditis
– Cardiac arrhythmia
– Negatively inotropic drug overdose (Beta blockers ir calcium channel blockers)
-Obstructive shock
– Tension pneumothorax
– Massive PE
– Cardiac tamponade
Reduced systemic vascular resistance (SVR):
-Septic shock
-Anaphylactic shock
-Neurogenic shock
How are BP, cardiac output, systemic vascular resistance, heart rate and stroke volume related
BP=COxSVR
CO=HRxSV
What is stroke volume
The volume of blood pumped by the heart per contraction
Determined by:
-preload
-myocardial contractility
-afterload
What is preload
The ventricular wall tension at the end of diastole and reflects the degree of myocardial muscle fibre stretch
Determined by volume status, venous capacitance and the difference between mean venous pressure and right arterial pressure
What is myocardial contractility
The intrinsic ability of the heart to work independently of preload and after load
What is afterload
Ventricular wall tension at the end of systole and is the resistance to anterograde blood flow
What is the pathophysiology of shock
Regardless of the cause of shock, inadequate organ perfusion tissue oxygenation results in cells switching from aerobic to anaerobic metabolism, generating a lactic acidosis that distrupts the cellular environment and causes myocardial depression
How is shock assessed
Assessment of severity:
-dyspnoea
-confusion
-light headedness
-drowsiness
-oliguria/anuria
-symptoms of the cause
O/E:
Airway:
-may be compromised due to reduced consciousness
Breathing:
-hypoxia secondary to::
– cause
– airway compromise
– apparent hypoxia due to pulse oximetry ineffective from peripheral shutdown
-tachypnoea
-Kassmaul’s breathing (hyperventilation to compensate for metabolic acidosis manifesting as “air hunger”)
Circulation:
-Cold, pale peripheries
-prolonged cap refill >2s
-Tachycardia
-Hypotension
-Oliguria
-Anuria
Disability:
-Confusion
-drowsiness
-unconsciousness
Signs of cause
Investigations:
-Bloods inclusing blood gas to check lactate
-ECG
-CXR
-Echo
-In trauma:
– Pelvic XR
– CT chest/abdo/pelvis as indicated
– FAST
How is haemorrhagic shock classified
Type I
-Volume of blood loss (ml): <750
-Percentage blood loss (%): <15
-Heart rate (beats/min): <100
-Blood pressure: normal
-Pulse pressure: normal/increased
-Respiratory rate (breaths/min): 14-20
-Urine output (ml/hour): >30
-Mental state: slightly anxious
Type II
-Volume of blood loss (ml): 750-1500
-Percentage blood loss (%): 15-30
-Heart rate (beats/min): 100-120
-Blood pressure: normal
-Pulse pressure: decreased
-Respiratory rate (breaths/min): 20-30
-Urine output (ml/hour): 20-30
-Mental state: mildly anxious
Type III
-Volume of blood loss (ml): 1500-2000
-Percentage blood loss (%): 30-40
-Heart rate (beats/min): 120-140
-Blood pressure: decreased
-Pulse pressure: decreased
-Respiratory rate (breaths/min): 30-40
-Urine output (ml/hour): 5-15
-Mental state: anxious, confused
Type IV
-Volume of blood loss (ml): >2000
-Percentage blood loss (%): >40
-Heart rate (beats/min): >140
-Blood pressure: decreased
-Pulse pressure: decreased
-Respiratory rate (breaths/min): >35
-Urine output (ml/hour): negligible
-Mental state: confused, lethargic
How is shock managed
Initial:
ABCDE assessment
Airway management
High flow 02 non-rebreathe to >94% sats
Obs monitoring
Three lead cardiac monitoring
ECG request
Portable CXR
Large bore IV access and take bloods and blood gas
Fluid resuscitation IV
Catheterisation and fluid balance monitoring (aiming output >0.5ml/kg/hr)
If BP fails to respond, refer to HDU/ICU for:
- central line insertion with central venous pressure and central venous oxygen saturation monitoring
- arterial line insertion and invasive arterial BP monitoring
- vasopressor and/or inotrope infusion
Further:
Identify and treat the cause:
-Haemorrhagic
– identify bleed and acheive control
– restoration of adequate circulating volume
— crossmatch blood and activate major haemorrhagic protocol
— transfuse o neg until cross matched blood available (ASAP)
– Correct coagulopathy by transfusion of platelets, fresh frozen plasma and cryoprecipitate as appropriate
-Septic
– antibiotics
– source control
-Anaphylactic
– adrenalin 0.5mg IM
-Tension pneumothorax
– needle thoracentesis
– intercostal chest drain insertion
-Cardiac tamponade
– Pericardiocentesis
– Thoracotomy
-Massive PE
– Thrombolysis
-Unstable tachyarrhythmias
– Synchronised direct current cardio version
-Unstable bradyarrhythmias
– Pacing
How will overdose/ poisoning present
Usually immediately after an accidental ingestion or inhalation of known drug or chemical but may present later in intential overdose
Acute confusional states
Hypoglycaemia
Abnormal liver function tests
Unexplained seizures
Abnormal bleeding
Several close contacts presenting with similar symptoms such as headache and confusion - ?CO poisoning in house
Recurrent or chronic unexplained symptoms in children (deliberate poisoning in Munchausen by proxy or factitious disorder)
What are the signs and symptoms of paracetamol overdose
Frequently asymptomatic
Symptoms:
Nausea and vomitting
Anorexia
Malaise
Abdominal pain
Altered mental status
Confusion
Evidence of previous self harm eg scars
Signs:
Asterixis
Bruising
Jaundice
Right upper quadrant pain
Oliguria/ anuria
Tachycardia/ hypotension
Coma
When is liver damage maximal in paracetamol overdose
3-4 days after overdose and may lead to liver failure, hypoglycaemia, encephalopathy, coma and death
How does aspirin overdose present
Hyperventilation
Tinnitus
Deafness
Vasodilation
Sweating
Coma in severe poisoning
How does tricyclic and related antidepressant overdose present
Dry mouth
Seizures
Coma
Cardiac conduction defects and Arrhythmias
Hypothermia
Hypotension
Hyperreflexia
Extensor plantar response
Convilsions
Respiratory failure
Dilated pupils
Urinary retention
How does SSRI overdose present
Nausea
Vomiting
Agitation
Tremor
Nystagmus
Drowsiness
Sinus tachycardia
Convulsions
Hyperthermia
Rhabdomyolysis
Renal failure
Coagulation deficiencies
Rarely can result in serotonin syndrome with marked neuropsychiatric effects, autonomic instability and neuromuscular hyperactivity
How does beta blocker overdose present
Bradycardia
Hypotension
Syncope
Conduction abnormalities
Heart failure
Drowsiness
Confusion
Convulsions
Hallucinations
Coma (in severe cases)
How do calcium channel blocker overdoses present
Nausea and vomiting
Agitation
Confusion
Dizziness
Coma
Metabolic acidosis and hyperglycaemia
Peripheral vasodilation and severe hypotension (in dihydropyridine calcium channel blockers)
Arrhythmias including heart block and asystole (Verapamil and diltiazem)
How does iron overdose present
Nausea
Vomiting
Diarrhoea
Abdominal pain
Haematemasis
Rectal bleeding
Hepatocellular necrosis and hypotension can occur later
Coma, shock and metabolic acidosis (in severe cases)
How does lithium toxicity present
Most offten in patients on long-term lithium and whose excretion of lithium is reduced due to dehydration or infection etc
Delayed onset of symptoms in deliberate overdose (12 hours or more)
Initially:
-apathy
-restlessness
Followed by:
-vomiting
-diarrhoea
-ataxia
-tremor
-weakness
-dysarthia
-muscle twitching
Severe poisoning:
-electrolyte imbalance
-dehydration
convulsions
-renal failure
-hypotension
-coma
How does opioid overdose present
Drowsiness
Coma
Respiratory depression
Pinpoint pupils
