A&E Flashcards
Acid Base Abnormalities
Aetiology
Clinical Presentation
Investigations
Management
Complications
Conditions characterised by changes in the conc of H + ions or bicarbonate HCO3- leading to arterial blood pH
Metabolic Acidosis
Anion Gap is Na + K - (CL+ HCO3) (minus the negative ions )
- Normal Anion Gap (6-16mmol/L): excreting HCO3-in GI or kidneys not excreting H+ for example, diarrhoea, renal tubular acidosis, addisons disease (hyperkalaemia = acidosis), acetazolamide , spironalactone
- Raise Anion Gap (over 16mmol/L): lactic acidosis (sepsis, metformin), diabetic ketoacidosis, uraemia, alcohol (metabolic ketoacidosis w/ normal or low glucose), (aspirin LATE stage)
Metabolic Alkalosis: loss H+ or gain HCO3- for example, vomiting, diuretics, hyperaldosteronism + cushings (hypokalaemia= high HCO3-)
Respiratory Acidosis: hypoventilation: airway obstructions, COPD, opioids/sedatives, weakened respiratory muscles
Respiration Alkalosis: hyperventilation: anxiety/panic attack, PE, hypoxia (high altitude), acute aspirin OD
ABG
if pH and HCO3 are both raised or lowered then metabolic
if pH and CO2 are in opposite direction then think respiratory
base excess= over 3 means metabolic alkalosis, less than 3 is metabolic acidosis
if respiratory then treat cause
if metabolic
- acidosis→ IV sodium bicarbonate
- alkalosis → acetazolamide (carbon anhydrase inhibiting diuretic)
Anaphylaxis
Aetiology
Clinical Presentation
Investigations
Management
Complications
Acute, life-threatening type 1 hypersensitivity reaction due to IgE mediated mast cell activation
Cause: food allergies, insect stings, drug reactions (penicillin, latex)
Degranulation of Mast Cells cause massive histamine release→ Systemic Vasodilation→ Increased Capillary Leakage→ Anaphylactic shock
RF: history of atopy
Mast-Cell Tryptase- elevated for up to 12h after onset
ECG, U+E, ABG- routine bloods and investigation
- Acute onset
- Airway swelling (angio-oedema)
- Stridor (noisy breathing through obstructed airway)
- dyspnoea
- wheezing
- resp arrest
- Pale, clammy skin
- hypotension
- tachycardia
- confusion
- Urticaria, erythema
- Pruritus
ABCDE approach + high flow oxygen 15L/mins non-rebreathe
1- remove the trigger + call for help
ASAP: IM adrenaline (500mcg dose of 0.5ml 1:1000IM adrenaline for adults in anterolateral medial thigh). 6-12 yrs old = 300mcg, 6month - 6 yr = 150mcg, under 6 month =100-150.
Do IM even if IV is established
If refractory anaphylaxis : 2 doses of IM adrenaline but doesnt work then do IV adrenaline and IV fluid bolus
After adrenaline-
IV cetirizine 10-20mg OR chlorophenamine 10mg
consider if ongoing asthma/shock or refractory anaphylaxis : IV hydroscortisone 200mg
Complications → recurrence, cardiac arrest, distributive shock
Prognosis → outlook will depend on the success of immunotherapy, allergen avoidance, and compliance with carrying their adrenaline (epinephrine) auto-injectors
Extradural Haemorrhage
Aetiology
Clinical Presentation
Investigations
Management
Complications
Bleeding between skull and dura mater
Mostly male 20-30 years old
- Most cases are traumatic from head injury
- Most commonly arterial bleed- rupture of middle meningeal artery
- Pterion is common site of rupture- thinnest part of skull where middle meningeal artery lies
Present with sudden onset soon after injury following a brief lucid interval:
1) Initial loss of consciousness after head injury
2) temporary consciousness recovery & return to normal neurological function (lucid interval)
3) neurological status declines again due to haematoma expansion
See neurological deficits contralaterally to the bleed
Signs of raised ICP: headache and confusion
Compression of oculomotor nerve (CN3) → fixed, dilated pupils
Cushings reflex: Hypertension and bradycardia
INVESTIGATIONS
Non-contrast CT: Hyperdense (bright) biconvex lesion limited by suture lines (lemon shape)
MANAGEMENT
Emergency as haematoma expansion can lead to brain herniation and death
Craniotomy and haematoma evacuation
Need to manage ICP (hypertonic saline) and prevent haematoma expansion with anticoagulant reversal
Correction of coagulopathy can include vitamin K (useful in patients with warfarin-related prolongation of INR), fresh frozen plasma, platelets (goal platelet count is >100 x 10⁹/L; >100,000/microlitre), cryoprecipitate (used in patients with low fibrinogen levels), protamine (used for patients on heparin), and activated factor VIIa.
also need to give prophylactic anti epileptic for a week from presentation either phenytoin or levetiracetam
If asymptomatic/ haemorrhage under 10mm: Cautious clinical and radiological observation with prophylactic epileptics. Consider correcting coagulopathy and ICP management
PROGNOSIS
In patients with no other associated brain injury, early decompression is associated with good neurological outcomes, including full recovery
Respiratory Arrest
Aetiology
Clinical Presentation
Investigations
Management
Complications
Complete cessation of breathing in patients with a pulse
Extrapulmonary causes:
- CNS depression (opioid intoxication)
- Respiratory muscle weakness (myasthenia gravis, ALS)
- Airway obstruction (aspiration)
- Drowning
- Trauma
Pulmonary Causes:
- Airway obstruction (bronchospasm in asthma/COPD)
- Impaired alveolar diffusion (pulmonary oedema, pneumonia)
CLINICAL FEATURES
- Cyanosis
- Tachycardia
- Diaphoresis- excess sweating
- CNS impairment- altered mental status
INVESTIGATIONS:
ABG: Reduced O2, Increased CO2
Pulse oximetry
MANAGEMENT
If obstructed- airway clearance: Direct laryngoscopy or bronchoscopy may be required to clear an airway foreign body. Emergency cricothyroidotomy or tracheostomy may be needed to manage structural obstructions at the glottic or infra-glottic level. Acute treatment may be required to reduce the swelling of an airway blocked due to anaphylaxis.
Give supplemental oxygen too: by nasal cannula, mask, or non-invasive (positive pressure) ventilation (NIV)
If unstable:
- Supplemental Oxygen
- Mechanical ventilation
- Intubation
PROGNOSIS
- Hypoxic organ damage
- Cardiac arrest
Unstable Angina
Aetiology
Clinical Presentation
Investigations
Management
Complications
Myocardial ischaemia at rest or on minimal exertion in absence of acute cardiomyocyte injury/necrosis
Risk Factors:
- Diabetes
- Hyperlipidaemia
- Hypertension
- Obesity
- Metabolic syndrome
- Renal impairment
- PVD
- Advanced age
- Smoking
CLINICAL PRESENTATION
- Chest pain that comes on randomly
- Sweating
- Dyspnoea
- Syncope
INVESTIGATIONS
ECG- no changes
Troponin- not elevated
Chest X-ray- look if pulmonary cause
Bloods- LFTs u+Es, creatinine, FBC
MANAGEMENT
Aspirin 300mg (continue indefinitely) & Fondaparinux (antithrombin- if no immediate PCI (aka coronary angioplasty) planned)
calculate GRACE SCORE
if low risk less than 3%= Ticagrelor + aspirin
if high risk= Angiography with followup PCI if indicated, Give ticagrelor
suspected or confirmed unstable angina:
aspirin + fondaparinux,
Consider: GTN, morphine, prasugrel/ticagrelor/clopidogrel, anti-emetic,
GRACE score
After stabilised : beta blocker (bisprolol), GTN, continue aspirin + prasugrel/ticagrelor/clopidogrel
Consider: ACEi, statin, aldosterone, SGLT2
COMPLICATIONS
- Congestive heart failure
- Ventricular arrhythmias
- Treatment complications- bleeding or thrombocytopenia
PROGNOSIS
overall mortality for the non-ST-elevation acute coronary syndrome (NSTE-ACS) patient population is 4.8% over a 6-month period
