Emergency Flashcards
Anaphylaxis doses?
Adrenaline 0.5 mg 1:1000
Hydrocortisone 200mg IV
Chlorphenamine 10mg IV
Salbutamol 5mg neb
SIRS criteria?
HR >90
RR >20 or PaCO2 <4.3
Temp <36 or >38.3
WCC <4 or >12
Sepsis classification?
Sepsis = SIRS + known/suspected infection
Severe sepsis = sepsis + signs of hypoperfusion/organ failure
Septic shock = persistent hypotension despite adequate fluid resuscitation
Causes of cardiogenic shock?
Pump failure –> LV dysfunction, aortic dissection, dysrhythmia
Inadequate filling –> PE, pneumothorax, tamponade
What is Beck’s triad of cardiac tamponade?
Low BP
Raised JVP
Faint heart sounds
Causes of hypovolaemic shock?
Haemorrhage
Salt + water loss
3rd space loss
ABG result in vomiting and haemorrhage?
Vomiting = alkalosis
Haemorrhage = acidosis
Definitions of respiratory failure?
Type 1 = PaO2 <8 kPa, PaCO2 <6.5 kPa
Type 2 = PaO2 <8 kPa, PaCO2 >6.5 kPa
Causes of type 1 respiratory failure?
V/Q mismatch
Obstructed airways = asthma, COPD
Block in blood flow = PE
Pulmonary oedema, ARDS
Why is CO2 normal in type 1 RF?
Because areas that are perfused and ventilated can blow it off by increasing RR
Causes of T2RF?
Alveolar hypoventilation - O2 can’t get in and CO2 can’t get out
Reduced ventilatory effort, increased dead space, increased CO2 production
Severe asthma –> exhaustion
Acute epiglottitis
Respiratory muscle paralysis
Signs of hypoxia?
Restlessness, confusion –> coma
Signs of hypercapnia?
Drowsiness Flapping tremor Warm peripheries Headaches Bounding pulses Papilloedema
Oxygen therapy in T1RF?
Unrestricted (35%+)
Repeat gases after 20 mins to ensure correction of PaO2 and absence of rise of PaCO2
Oxygen therapy in T2RF?
Controlled (start at 24% and titrate)
Monitor PaCO2 closely by repeat gases - if it rises by more than 1 kPa, consider NIV
Contraindications to NIV?
Inability to protect airway Cardiac/respiratory arrest Upper airway obstruction Pneumothorax Haemodynamic instability Maxillofacial surgery Basal skull fracture Intractable vomiting
When is CPAP used?
Acute pulmonary oedema
Asthma
Obstructive sleep apnoea
When is BIPAP used?
COPD
Weaning
Asthma
Neuromuscular disease
PCM OD dose associated with hepatic necrosis?
250 mg/kg
Clinical features of PCM overdose after 24h?
RUQ pain +/- evidence of liver failure
PT, ALT, AST - raised
PT/INR is best marker of synthetic function
Clinical features of PCM overdose after 3-5 days?
Recovery may begin, or fulminant hepatic failure
Cogagulopathy
Hypoglycaemia
Encephalopathy
AKI (hepatorenal syndrome)
ABG in PCM overdose?
pH <7.3 despite fluid resuscitation predicts mortality
Management of PCM overdose? (levels)
<4 hrs - take levels and wait
4-8hrs - take levels and treat if over treatment line
8-15hrs - treat before levels come back, stop if under treatment line
> 15hrs/staggered - treat
Doses of parvolex/NAC?
150 mg/kg in 200ml over 1 hour
50 mg/kg in 500ml over 4 hours
100 mg/kg in 1000ml over 16 hours
When to discontinue NAC?
If plasma concentration later reported to be below treatment line and patient is asymptomatic with normal LFTs, creatinine and PT.
Side effects of NAC?
20% have pseudoallergic (anaphylactoid) reaction
stop infusion and give chlorphenamine
Pathophysiology of salicylate overdose?
Acid base disturbance
Uncoupling of oxidative phosphorylation
Disordered glucose metabolism
Signs/symptoms of salicylate overdose?
N+V, abdominal pain, tinnitus
Deafness, hyperventilation, flushed skin, sweating, hyperthermia
Complications of salicylate overdose?
Aspiration Pulmonary oedema Cardiovascular instability Hypo/hyperglycaemia Hypokalaemia Hypoprothrombinaemia Thrombocytopenia DIC Renal failure
Salicylate levels?
Mild - <500mg/L
Moderate - 500-750 mg/L
Severe - >750 mg/L
ABG in salicylate overdose?
Metabolic acidosis (lactate) Respiratory alkalosis (hyperventilation)
ECG in salicylate overdose?
Widened QRS
AV block
Ventricular dystrhythmias
Bloods in salicylate overdose?
Glycaemic, Electrolytes, Bleeding, Renal
Hypo/hyerglycaeima Hypokalaemia Hypoprothrombinaemia Thromboyctopenia DIC Renal failure
Correcting acid-base, electrolyte, bleeding abnormalities in salicylate overdose?
Glucose infusion if hypoglycaemic
Correct electrolytes
Vitamin K if hypoprothrombinaemia
Sodium bicarb for severe acidosis
Dialysis in moderate-severe cases
Pathophysiolog and dose of TCA overdose?
TCA = sodium-channel blocking agent –> seizures and ventricular dysrhythmias
10mg/kg potentially life threatening, 30mg/kg –> severe toxicity
Rapid deterioration within 1-2 hours of ingestion
CNS, CVS and anticholinergic features of TCA overdose?
Sedation/coma/convulsions/delirium - FIRST
Sinus tachy + HTN –> hypotension
Broad complex tachydysrhythmia –> broad complex bradycardia (pre-arrest)
Agitation, restlessness, delirium, mydriasis, dry, warm flushed skin, urinary retention, tachycardia, ileus, myoclonic jerks
ABG/ECG findings in TCA overdose?
Metabolic acidosis
Prolonged PR
Wide QRS/QTc
RAD of terminal QRS
Ventricular dyshythmia
Management of TCA overdose?
Sodium bicarb IV - bolus every few minutes until BP improves and QRS narrows
SEIZURES
IV benzos, sodium bicarb, RSI/ventilation
HYPOTENSION
IV crystalloid bolus, vasopressors (ICU)
CNS DEPRESSION
Intubation - hyperventilate to pH 7.5-7.55
Effects of iron overdose? (Local and systemic)
LOCAL (GI)
Corrosive injury to mucosa –> D+V, haematemesis, melena, fluid losses –> hypovolaemia
SYSTEMIC
Iron = cellular toxin, targets CVS and liver.
Secondary CNS effects
Metabolic acidosis due to hyperlactemeia and free proton production from hydration of free ferric ions
Coagulopathy
Risk assessment of iron overdose?
<20 mg/kg = asymptomatic
20-60 mg/kg = GI symptoms only
60-120 mg/kg = potential for systemic toxicity
>120 mg/kg = potentially lethal
Iron overdose presentation?
0-6 HOURS
vomiting, diarrhoea, haemetemesis, melena, abdominal pain. Significant fluid losses –> hypovolemic shock
6-12 HOURS
GI symptoms wane and the patient appears to be getting better. During this time iron shifts intracellularly from the circulation
12-48 HOURS
Cellular toxicity becomes manifest as vasodilative shock and third-spacing, high anion gap metabolic acidosis (HAGMA) and hepatorenal failure
2-5 DAYS
Acute hepatic failure, although mortality is rare
2-6 WEEKS
Chronic sequelae occur in survivors –– cirrhosis and gastrointestinal scarring and strictures
Serum iron concentration levels in iron overdose?
Peak levels after 4-6 hours
Levels fall after 6 hours due to intracellular shift
90 micromol/L = systemic toxicity
Blood gas in iron overdose?
HAGMA = high anion gap metabolic acidosis
Useful marker of systemic toxicity
Managment of iron overdose?
ABCDE = priority –> restoration of circulating volume
Decontamination - whole bowel irrigation or surgical/endoscopic removal if lethal ingestion
Antidote in iron overdose?
DESFERRIOXAMINE
Chelates free ferric and ferrous ions –> water soluble complexes that can be renally excreted
Cardiac monitoring mandatory when infusion running
ECG findings in hypothermia?
brady J wave 1st degree heart block Long QT Arrhythmias
Presentation of delirium?
New change in…
Cognition/concentration Physical function Social behaviour Appetite, sleep, mood Hallucinations Falls
Causes of delirium?
DELIRIUM
Drugs (withdrawal/toxicity, anticholinergics)/Dehydration
Electrolyte imbalance/Environmental factors
Level of pain
Infection/Inflammation (post surgery)
Respiratory failure (hypoxia, hypercapnia)
Impaction of faeces
Urine retention
Metabolic disorder (liver/renal failure, hypoglycaemia)/Myocardial infarction
General measures for delirium?
Calming environment
Rationalise medications
Hydrate (oral best)
Monitor bowls/treat constipation
Frequently reassure/reorientate
Optimise sensory impairment (glasses, hearing aid)
Look for and treat infection
Don’t argue/confront, move bays, restrain or do unnecessary procedures
Indications for sedation in delirium?
Carry out essential investigations
Prevent danger to self or others
Relieve patient distress
Sedation agents in delirium?
Haloperidol 0.5mg PO, 1-2 hourly, max 5mg daily
Can add lorazepam - avoid due to hangover effect/dependence
When should benzos be first line for sedation?
Prolonged QRS, DLB, Parkinson’s
Seizures, rec drug intoxication/withdrawal, alcohol withdrawal
What is spinal shock?
Loss of sympathetic vascular tone –> dilation of arterioles/venous pooling –> low BP and low CO
Loss of sympathetic drive to heart (T1-T4)
Causes of spinal shock?
Traumatic - transection of spinal cord at any level
Iatrogenic - final spinal anaesthesia
Symptoms and signs of spinal shock?
Motor/sensory dysfunction below level of lesion (UMN lesion) + bladder/bowl dysfunction
Low BP, warm peripheries, may not be able to mount tachycardia if lesion above T1-T4
Focal neurology +/- up going plantars, loss of anal tone
What are complications of shock?
PROLONGED HYPOTENSION –> HYPOPERFUSION
Brain - low CNS/coma
Kidneys - AKI/ATN
Liver - ischaemic hepatitis
Heart - myocardial ischaemia/MI
Definition of AKI?
Rise in serum creatinine >26µmol/L within 48hrs or rise in serum creatinine 1.5 x baseline value within 1wk or urine output <0.5ml/kg/hr for 6hrs.
AKI staging systems?
RIFLE
AKIN
KDIGO
AKI Management? ABCCDD
Assess (fluid balance) Bloods (K+, urea, cr) Catheter Cannula (IV fluids) Drugs (check chart) Dialysis?
Drugs to stop in AKI?
ACEi
Metformin
Diuretics
NSAIDs
Indications for RRT in AKI?
Uraemic complications (enceph, pericarditis)
Refractory Pulmonary oedema
Refractory metabolic acidosis
Refractory hyperkalaemia
HAGMA and NAGMA?
HAGMA = accumulation of organic acids/impaired H+ excretion (LKTR - lactate, toxins, ketones, renal)
NAGMA = loss of HCO3- from ECF (hyperchloraemia, acetazolamide/addison’s, GI losses)
