Emergency Medicine Flashcards
1st line for opiod overdose
Naloxone
1st line for opiod detoxification
Methadone/ buprenorphine
Posterior hip dislocation presentation
Shortened, adducted and internally rotated leg
Anterior hip dislocation
Abducted and externally rotated leg, no leg shortening
Achilles tendon rupture presentation
- increased resting ankle dorsiflexion in a prone position with knees bent
- a palpable gap above the heel
- a lack of plantar flexion when the calf is squeezed (Thompson’s test positive)
Achilles tendon rupture investigation
Ultrasound scan
Pulmonary embolism presentation
- pleuritic chest pain
- dyspnoea
- haemoptysis
Signs: - tachypnea
- crackles
- tachycardia
- fever
Left ventricular free wall rupture presentation
Sudden heart failure, raised JVP, pulsus parodoxus, recent MI
Multiple myeloma presentation
- around 70yrs old
- C - Hypercalcaemia
- R - Renal damage (dehydration/ thrist)
- A - Anaemia
- B - Bleeding/ bruising
- B - Bones (pain, fractures)
- I - Infection
Multiple myeloma investigations
- full blood count: anaemia
- peripheral blood film: rouleaux formation
- urea and electrolytes: renal failure
- bone profile: hypercalcaemia
Anaphylaxis presentation
- lips/ tongue/ airway swelling
- dyspnoea
- wheeze
- chest tightness
- pruritus
- erythmema
- urticaria
- peripheral vasodilation
- N/V, diarrhoea
Anaphylaxis management
- give oxygen
- open and maintain airway
- 0.5mg IM adrenaline
- nebulised salbutamol for bronchospasm
Diabetic ketoacidosis aetiology
- insulin deficiency:
– undiagnosed DM
– interrupted insulin therapy
– intercurrent illness - eg. infection or surgery
Diabetic ketoacidosis pathophysiology
- insufficient insulin -> increased hepatic gluconeogenesis -> high blood glucose -> osmotic diuresis -> dehydration
- increase in peripheral lipolysis -> free fatty acids -> liver converts to ketones -> metabolic (keto)acidosis
- no insulin to drive K into cells -> high serum K, low body K -> potassium imbalance
Diabetic ketoacidosis presentation
- Polyuria
- Polydipsia
- Nausea and vomiting
- Acetone smell to their breath
- Kussmaul respiration (deep hyperventilation)
- Dehydration
- Weight loss
- Hypotension (low blood pressure)
- Altered consciousness
- Abdominal pain
Diabetic ketoacidosis diagnostic criteria
- Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
- Ketosis (e.g., blood ketones above 3 mmol/L)
- Acidosis (e.g., pH below 7.3)
(metabolic acidosis with a low bicarbonate)
Diabetic ketoacidosis invesstigations
- blood glucose
- blood ketones
- venous blood gas
- urine dipstick
- U & Es
- FBC
- identifying a precipitating cause (eg blood cultures/ MSU for infection)
Diabetic ketoacidosis management
- IV fluid resus with normal saline (1L/1st hour-> 1L/2hourly)
- fixed-dose IV insulin therapy (0.1units/kg/hr)
- monitor blood glucose, if < 14mmol/L add 10% dextrose at 125ml/hr
- add KCl to fluids if needed (K<5.5) upto 20mmol/hr
- treat underlying triggers (eg infection)
- monitor blood ketones, pH and bicarbonate
- continue long-acting, stop short-acting insulin
Diabetic ketoacidosis resolution
- pH >7.3 and
- blood ketones < 0.6 mmol/L and
- bicarbonate > 15.0mmol/L
- pt should be eating/ drinking
- pt should have started regular SC insulin
ACVPU scale
- Alert
- Confusion (new-onset)
- Voice
- Pain
- Unresponsive
3 types of paracetamol overdose
- Acute overdose: excess amounts of paracetamol ingested over less than one hour, usually in the context of self-harm
- Staggered overdose: excess amounts of paracetamol ingested over longer than one hour, usually in the context of self-harm
- Therapeutic excess: excess paracetamol ingested with the intent to treat pain or fever and without the intent of self-harm
Paracetamol overdose early presentation
Early (<12hrs):
* Potentially asymptomatic
* Nausea and vomiting
* Mild/moderate abdominal pain/tenderness
Paracetamol overdose pathophysiology
- paracetamol metabolised by cytochrome P450 enzymes into toxic NAPQI
- usually NAPQI conjugated with glutathione for excretion
- excess NAPQI = insufficient glutathione -> NAPQI damages hepatocytes -> acute liver failure -> death
Paracetamol overdose late presentation
Late (12-36hrs):
* Moderate/severe abdominal pain
* Metabolic acidosis
* Jaundice
* Acute kidney injury
* Hepatic encephalopathy
* Coma
* Bruising or systemic haemorrhage may indicate coagulopathy secondary to impaired hepatic clotting factor production
Paracetamol overdose investigations
- Paracetamol concentration
- Liver function tests
- INR
- Urea and electrolytes
- Plasma bicarbonate
- Plasma glucose
- Full blood count
Paracetamol overdose investigations
- accurate history essential:
– combination/ strength ingested
– length of time ingested over
– time since ingestion - activated charcoal if present within 1hr
- IV acetylecysteine given over 1hr if:
– staggered overdose
– present 8-24hrs
– present >24hrs if jaundiced/ hepatic tenderness
– plasma paracetamol conc. on/ above single treatment line
Rhabdomyolysis pathophysiology
breakdown of skeletal muscle cells -> release of intracellular fluids (CK, myoglobin, urate, electrolytes) into circulation -> electrolyte imbalances/ AKI
Rhabdomyolysis aetiology
- seizure (esp status epilepticus)
- collapse/coma (prolonged immobilisation)
- ecstasy
- crush injury
- McArdle’s syndrome (genetic disorder)
- drugs: statins (especially if co-prescribed with clarithromycin)
Rhabdomyolysis presentation
- AKI with raised creatinine
- significantly elevated CK
- myoglobinuria: (tea-coloured)
- hypocalcaemia (myoglobin binds calcium)
- elevated phosphate (released from myocytes)
- hyperkalaemia (may develop before renal failure)
- metabolic acidosis
Rhabdomyolysis management
- IV fluids to maintain good urine output
- manage any electrolyte disturbances
- urinary alkalinization in severe cases (IV sodium bicarb)
Total anterior circulation stroke
- Unilateral weakness (and/or sensory deficit) of the face, arm and leg
- Homonymous hemianopia (loss of half of the visual field in both eyes)
- Higher cerebral dysfunction (dysphasia, visuospatial disorder)
Partial anterior circulation stroke
TWO of the following:
* Unilateral weakness (and/or sensory deficit) of the face, arm and leg
* Homonymous hemianopia (loss of half of the visual field in both eyes)
* Higher cerebral dysfunction (dysphasia, visuospatial disorder)
OR higher cerebral dysfunction alone
Posterior circulation syndrome
- Cranial nerve palsy with a contralateral motor or sensory deficit, or
- Bilateral motor/sensory deficit, or
- Conjugate eye movement disorder, or
- Symptoms of cerebellar dysfunction such as vertigo, nystagmus or ataxia, or
- Isolated homonymous hemianopia
Stroke differentials
- Seizures (Todd’s paresis)
- Migraine
- Bell’s palsy
- Vestibular neuritis / BPPV
- Head injuries
- Exacerbation of an old stroke
- Space-occupying lesions (e.g. tumours)
- Demyelinating disorders (e.g. multiple sclerosis)
- Delirium
- Sepsis and central nervous system infections
- Hypoglycaemia and hyperglycaemia
- Intoxication with alcohol or drugs
Ischaemic stroke management
- aspirin 300mg, cont. 2 weeks
- thrombolysis with alteplase within 4.5hrs of onset
- thrombectomy within 6-24hrs if confirmed PAC
- stroke rehab if needed
secondary prevention: - clopidogrel/ dipyridamole
- treat modifiable RF (eg HTN)
Burns immediate management (heat/ electrical/ chemical)
- airway, breathing, circulation
- burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
- electrical burns: switch off power supply, remove the person from the source
- chemical burns: brush any powder off then irrigate with water
How to assess the extent of a burn
- Wallace’s Rule of Nines: head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, anterior abdomen = 9%, posterior abdomen = 9%
- Palmar surface for smaller areas (SA of patients entire hand = 1%)
- Lund and Browder chart: the most accurate method
Burn depth classification
- Superficial (1st degree): Only epidermis damaged
- Superficial Partial (2nd degree): Epidermis & upper dermis damaged
- Deep Partial (2nd degree): Epidermis, upper & lower dermis damaged
- Full Thickness (3rd degree): All skin layers to subcutaneous tissues damaged
How to assess the depth of a burn
- superficial: Red and painful, dry, no blisters
- superficial partial: Pale pink, painful, blistered. Slow capillary refill
- deep partial: Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
- full thickness: White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
Severe burns pathohysiology
- local progressive tissue loss/ damage
- loss of capillary membrane integrity -> plasma leakage into interstitial space -> hypovolaemic shock (up to 48h after injury) - decreased blood volume and increased haematocrit
- Immunosuppression is common -> high risk of sepsis
Severe burns management
- stop burning process
- assess airway - consider early intubation (eg smoke inhalation/ deep facial burns/ blisters to oropharynx)
- IV fluids: children with burns >10% of total body surface area, adults with burns >15% TBSA
- urinary catheterisation
- analgesia
- transfer to burns unit if complex
8 reversible causes of cardiac arrest
4Hs and 4Ts:
* Hypoxia
* Hypokalaemia/hyperkalaemia
* Hypothermia/hyperthermia
* Hypovolaemia
* Tension pneumothorax
* Tamponade
* Thrombosis
* Toxins
Salicylate examples
- NSAIDs
- Aspirin
- Certain antacids and antidiarrhoeal meds
Salicylate overdose pathophysiology
- stimulate cerebral medulla -> hyperventilation -> respiratory alkalosis
- salicylate metabolisation -> uncoupling of oxidative phosphorylation -> anaerobic respiration -> increased lactate -> metabolic acidosis
- this results in a mixed respiratory alkalosis and metabolic acidosis
Salicylate overdose presentation
- hyperventilation (centrally stimulates respiration)
- tinnitus
- **lethargy
- sweating, pyrexia **
- nausea/vomiting
- hyperglycaemia and hypoglycaemia
- seizures
- coma
Salicylate overdose treatment
- general (ABC, charcoal)
- urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine
- haemodialysis
Describe the Monro-Kellie hypothesis
- the skull has a fixed capacity and contains 3 main substances: brain tissue, CSF and blood
- if the volume of 1 of these increases, the volume of one of the others must decrease to maintain a constant ICP (compliance)
- eg bleed in the brain = reduced CSF production
- once this compensatory compliance mechanism is overwhelmed, small increases in the volume of any one of the three substances will lead to dramatic increases in ICP
Raised ICP presentation
- Headache
- Nausea and vomiting
- Papilloedema
- Restlessness, agitation or drowsiness
- Slow slurred speech
- Ipsilateral sluggish dilated pupil which then becomes fixed (“blown pupil”)
- Cranial nerve palsy (e.g. CN III palsy with ‘down and out’ pupil)
- Seizures
- Reduced GCS
- Abnormal respiratory pattern
- Abnormal posturing, initially decorticate and then decerebrate
Cushing’s Triad
- Widening pulse pressure (inc. systolic, dec. diastolic)
- Bradycardia
- Irregular respirations
How to calculate cerebral perfusion pressure
- CPP = Mean Arterial Pressure (MAP) – ICP
Head injury: CT head in 1hr
- GCS < 13 on initial assessment
- GCS < 15 at 2 hours post-injury
- suspected open or depressed skull fracture
- post-traumatic seizure.
- focal neurological deficit.
- more than 1 episode of vomiting
- any sign of basal skull fracture
Head injury: CT head within 8hrs
LOC/ amnesia since injury, plus any of:
* age 65 years or older
* any history of bleeding or clotting disorders including anticogulants
* dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
* more than 30 minutes’ retrograde amnesia of events immediately before the head injury
Benzodiazepine overdose presentation
- Reduced level of consciousness (including coma): if severe this can result in loss of airway tone and reflexes leading to hypoxia if left untreated.
- Respiratory depression: decreased respiratory rate can result in hypoxia and inadequate tissue perfusion.
- Hypotension
- Bradycardia
- Rhabdomyolysis
- Hypothermia
Benzodiazepine overdose presentation
- Reduced level of consciousness (including coma): if severe this can result in loss of airway tone and reflexes leading to hypoxia if left untreated.
- Respiratory depression: decreased respiratory rate can result in hypoxia and inadequate tissue perfusion.
- Hypotension
- Bradycardia
- Rhabdomyolysis
- Hypothermia
Benzodiazepine overdose management
Flumazenil
Pulmonary embolism risk factors
- Recent surgery
- Recent fractures
- Recent immobility
- Personal or family history of a clotting disorder or PE/DVT
- Obesity
- Malignancy
- Infection
- Pregnancy
- Medications such as the combined oral contraceptive pill or hormone replacement therapy
Pulmonary embolism presentation
- Shortness of breath
- Pleuritic chest pain
- Cough
- Haemoptysis: secondary to infarcted lung tissue.
- Dizziness or syncope
Signs: - Tachypnea
- Crackles
- Tachycardia
- Fever
Pulmonary embolism management
PE Wells Score
* PE likely (>4): CTPA, interim DOAC
* PE unlikely (4 or less): D-Dimer -> positive result -> CTPA
Pneumothorax definition
collection of air between the parietal and visceral pleura of the lung
Pneumothorax symptoms
sudden onset:
* dyspnoea
* chest pain: often pleuritic
* sweating
* tachypnoea
* tachycardia
Pneumothorax management
- no SOB, <2cm rim of air on CXR: no tx required, F/U in 2-4 weeks
- SOB or >2cm rim of air on CXR: aspiration and reassess -> chest drain if needed
Tension pneumothorax pathophysiology
- thoracic trauma -> creates one-way valve, air let in but not out of pleural space
- trapped air creates pressure inside thorax -> pushes mediastinum across -> kinks big vessels -> cardiorespiratory arrest
Tension pneumothorax signs
- Tracheal deviation away from the side of the pneumothorax
- Reduced air entry on the affected side
- Increased resonance to percussion on the affected side
- Tachycardia
- Hypotension
Tension pneumothorax management
Insert a large bore cannula into the second intercostal space in the midclavicular line
ACS presentation
- Pain radiating to the jaw or arms
- Nausea and vomiting
- Sweating and clamminess
- A feeling of impending doom
- Shortness of breath
- Palpitations
ACS immediate management
- M - IV morphine
- O - oxygen if sats below 94 (aim 94-98)
- N - nitrate
- A - aspirin 300mg
Status epilepticus medical management
- 1st line: 4mg IV lorazepam (give buccal/ IM if no IV access)
- Repeat after 10 minutes
- Phenytoin/ levetiracetam/ sodium valproate infusion
Status epilepticus general management
- Secure airway (nasopharyngeal)
- Position pt on left side (aspiration risk)
- Give oxygen
- Glucose/ thiamine if indicated
- Medical management (BDZs)
Phenytoin cautions
- Risk of arrhythmias (avoid if cardiac problems)
Causes of upper GI bleed
- Peptic ulcers (the most common cause)
- Mallory-Weiss tear (a tear of the oesophageal mucosa)
- Oesophageal varices (secondary to portal hypertension in liver cirrhosis)
- Stomach cancers
Upper GI bleed presentation
- Haematemesis (vomiting blood)
- Coffee ground vomit (caused by vomiting digested blood with the appearance of coffee grounds)
- Melaena (tar-like, black, greasy and offensive stools caused by digested blood)
Glasgow-Blatchford Bleeding Score factors
- Haemoglobin (falls in upper GI bleeding)
- Urea (rises in upper GI bleeding)
- Systolic blood pressure
- Heart rate
- Presence of melaena
- Syncope
- Liver disease
- Heart failure
Group and save vs Crossmatch
- “Group and save”: the lab checks the patient’s blood group and saves a blood sample to match blood if needed
- “Crossmatch”: the lab allocates units of blood, tests that it is compatible, and keeps it ready in the fridge
Upper GI bleed initial management
ABATED:
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 x large bore cannula)
T – Transfusions are required
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
When to transfuse a pt
- Massive haemorrhage
- Active bleeding plus thrombocytopenia (plt<50)
- Give prothrombin complex concentrate if active bleeding + warfarin
Major haemorrhage definition
- 50% blood loss within 3 hours
- Blood loss at a rate >150ml/minute
- Loss of one blood volume over 24 hours
In an acute scenario, bleeding plus: - A blood pressure <90mmHg systolic
- A heart rate >110bpm
How to locate a haemorrhage
- On the floor (external wound)
and four more: - chest cavity (haemothorax)
- abdominal cavity (injury to a solid organ/ major blood vessel)
- pelvis (fracture)
- long bones (fracture)
Haemorrage management aims
- Stopping the bleeding (direct pressure, medical/ surgical mx)
- Replacing lost blood volume (give colloids, 1:1 ratio of units of plasma and RBC)
- Avoid lethal triad (hypothermia, acidosis, coagulopathy - keep pt warm, maximise oxygenation, avoid crystalloids)
COPD exacerbation management
- oxygen
- nebulised salbutamol/ ipratropium bromide
- consider NIV
- consider antibiotics
- corticosteroids
Moderate asthma attack features
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
Severe asthma attack features
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
Life-threatening asthma attack features
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Acute asthma management
- admit to hospital if life-threatening
- give oxygen if hypoxaemic
- SABA - nebulised if life-threatening
- oral prednisolone for >5 days, in addition to ICS
- ipratroprium bromide if no response to SABA/ steroids
- IV magnesium sulfate/ aminophylline - senior management
