Emergency Medicine Flashcards
1
Q
Benzodiazepine overdose management
A
IV fluids and monitoring
-AVOID Flumazenil
2
Q
Situation where flumazenil can be given for benzodiazepine OD
A
- Unintentional lone paediatric benzodiazepine ingestion with compromised airway and breathing
- When benzodiazepine overdose results in compromised airway or breathing in
settings where resources for intubation are not available - Iatrogenic over-treatment with benzodiazepine
- An elderly patient with respiratory disease/ intubation should be avoided
Here are simplified situations where flumazenil can be given for a benzodiazepine overdose:
-
Child accidentally takes benzodiazepines and can’t breathe properly:
- Flumazenil can help reverse the overdose if the child’s breathing is compromised.
-
Overdose causes breathing problems where intubation isn’t possible:
- Flumazenil may be used when there’s no access to intubation equipment to help restore normal breathing.
-
Too much benzodiazepine given by mistake:
- Flumazenil can be administered to counteract the excessive dose.
-
Older patient with breathing issues; avoid intubation if possible:
- Flumazenil can help an elderly patient with respiratory disease by reversing the overdose effects without needing intubation.
3
Q
Cocain overdose treatment
A
1st: Sub-lingual nitro-glycerine
2. Benzodiazepines
NOTE: BB and aspirin are contraindicated
4
Q
Gram -ve organisms
KEPH
A
H influenzae
P aeruginosa,
K pneumoniae,
Escherichia coli
5
Q
Gram +ve organisms
SS
A
S pneumoniae
Staphylococcus aureus
6
Q
paracetamol overdose management
A
- < 2 hours: activated charcoal
2-8 hours: paracetmaol concentration + ALT and if serum concentration low, no treatment
If concentration high: IV N-acetyl cysteine - > 8 hours: IV N-acetyl cysteine
7
Q
Metabolic effects of aspirin overdose
A
– Early primary respiratory alkalosis.
– Late metabolic acidosis.
– Hypokalaemia.
– Hypoglycaemia-sometimes hyperglycaemia
An overdose of aspirin can cause a range of metabolic effects that change over time:
- Early primary respiratory alkalosis: Initially, aspirin stimulates the brain to cause rapid breathing, leading to a loss of carbon dioxide and resulting in respiratory alkalosis (higher pH due to lower CO2).
- Late metabolic acidosis: As the overdose progresses, the body accumulates acidic substances (like lactic acid and salicylic acid from the breakdown of aspirin), leading to metabolic acidosis (lower pH due to increased acids).
- Hypokalaemia: Aspirin overdose can cause low potassium levels in the blood (hypokalaemia), which can affect muscle and heart function.
- Hypoglycaemia or sometimes hyperglycaemia: Blood sugar levels can drop (hypoglycaemia) due to increased metabolic demands, but in some cases, they may rise (hyperglycaemia).
8
Q
hyperkalaemia treatment
A
- Calcium chloride
- sodium bicarbonate
- glucose/insulin
- haemodialysis
9
Q
Tampon + diffuse rash + fever + confusion + hypotension + multiorgan damage
A
Toxic shock syndrome
- Staph aureus
10
Q
Anaphylactic shock management
A
0.01ml/kg adrenaline IM
- IV hydrocortisone + antihistamine
11
Q
type 2 DM + hyperglycaemia + dehydration with/o
ketoacidosis
A
hyperosmolar hyperglycaemia
The key diagnostic difference between hyperosmolar hyperglycemic state (HHS) and diabetic ketoacidosis (DKA) is the presence of ketones and blood acidity:
- HHS: Very high blood sugar (usually above 600 mg/dL) with little to no ketones and normal or mildly increased blood acidity.
- DKA: High blood sugar (usually between 250-600 mg/dL) with high levels of ketones and significantly increased blood acidity.
12
Q
hyperosmolar hyperglycaemia treatment
A
Sodium (corrected) = Sodium (measured)
+ glucose / 4 (all values in mmol/L)
- if Na > 150 = sodium chloride 0.45%
13
Q
Diabetic ketoacidosis management
A
- IV saline 1 to 3 L of 0.9%
- insulin
- Dextrose 5%
14
Q
gliclazide + reinal impairment fixed by glucose infusion
A
sulphonylurea-induced hypoglycaemia
- IV glucose (5% dextrose) infusion for several days
15
Q
haemorrhage + lung Edema with/o
parenchymal disruption + several hours after the initial injury
A
Pulmonary contusion
16
Q
Pulmonary contusion management
A
Supporative
- good oxygenation
- adequate pulmonary toilette
Pulmonary contusion is a form of lung injury characterized by bruising of the lung tissue, typically resulting from blunt chest trauma. This injury leads to bleeding and swelling within the lungs, which can impair gas exchange and cause respiratory distress. Here are some key points about pulmonary contusion:
- Causes: Commonly results from blunt trauma, such as car accidents, falls, or sports injuries. It can also occur in situations involving blast injuries or severe compressive forces.
- Symptoms: May include chest pain, shortness of breath, coughing (sometimes with blood), and reduced oxygen levels in the blood. The severity of symptoms can vary depending on the extent of the injury.
- Diagnosis: Typically diagnosed using imaging studies like chest X-rays or CT scans, which can reveal areas of lung bruising and other associated injuries.
- Treatment: Management depends on the severity of the contusion. Mild cases may require only supportive care, such as oxygen therapy and pain management. Severe cases might necessitate mechanical ventilation and intensive care to ensure adequate oxygenation and ventilation.
- Prognosis: Varies based on the extent of the injury and the presence of any other associated injuries or complications. Most mild to moderate contusions resolve with appropriate treatment, but severe cases can lead to significant morbidity or even mortality, especially if not promptly and properly managed.
- Complications: Can include pneumonia, acute respiratory distress syndrome (ARDS), and respiratory failure, particularly in more severe cases or if the contusion is part of a broader traumatic injury.
17
Q
Diabetic ketoacidosis investigation
A
- Capillary blood sugar level
- Venous or arterial blood gases
- Blood or urinary ketone level
- Other investigations like chest X-ray, blood culture, urine culture, full blood count etc
18
Q
Chest trauma + Dyspnoea + Hypotension + Hyper-resonance + mediastinal shift
A
Tension pneumothorax
19
Q
Tension pneumothorax
A
needle thoracotomy
- chest tube after patient stable with needle
20
Q
Difference between pneumothorax vs haemothorax
A
pneumothorax: high percussion resonance
haemothorax: dull percussion resonance
21
Q
best indicator of an effective CPR
A
- Pupil size and reaction to light
- carotid and femoral pulse
22
Q
Nausea and vomiting + Excessive sweating + severe headache + Coagulation defects (raised INR,
APTT, bleeding). After attack
A
Snake envenomation
23
Q
Snake envenomation management
A
- Apply pressure immobilisation/elastic bandage (PIB)
- Check sign for envenomation
3: No envenomation: topical anaesthetics & swab bites
check labs for envenomation: if no signs release PIB, repeat blood test post removal if PIV, then 6 and 12 hours
4: If clinical envenomation present: 2 IVs + take bloods - Resuscitate
- Prep for anaphylactic reaction
- Give antivenom (1 vial tiger, 1 of brown)
- Release PIB after antivenom
24
Q
Medication that can cause angioedema
A
ACE1 30%
ARBs
25
Angioedema treatment
1. Cease offending drug
2. steroids, antihistamines and epinephrine
26
Digoxin immune Fab indication for digoxin toxicity
- Ingested dose (more than 10 mg in adults, more than 4 mg in children).
- Cardiac arrest.
- Potassium concentration above 5.0 mmol/L.
- Life-threatening ventricular arrhythmias.
- Decompensation (hypotension) from bradyarrhythmia's
Digoxin immune Fab is used to treat severe digoxin toxicity. Digoxin toxicity happens when there's too much digoxin, a heart medication, in your body, which can cause dangerous heart problems. Digoxin immune Fab works by binding to the excess digoxin, making it inactive and helping your body safely get rid of it. This treatment quickly reduces the toxic effects and helps stabilize the heart.
27
severe dyspnoea + distress +
pallor + sweating + tachycardia + poor peripheral perfusion
X-ray: bilateral basal + mid zone whiteout
Acute Pulmonary oedema
28
Chronic digoxin toxicity
associated with intercurrent illness, (with impaired renal function)
symptoms of insidious onset over days to weeks
features: acute digoxin toxicity features with visual disturbances (e.g. reduced acuity, yellow halos (xanthopsia) and altered color perception (chromatopsia)
29
Cardiac arrest management
- Acidemic: compressions
- if hyperkaliaemic/ hypocalcaemic/ CCB OD: calcium gluconate injection
- TCA OD: Sodium bicarbonate
30
cardiac arrest core body temperature risk
32
31
altered mental status + sedation, tachycardia + signs of anticholinergic toxicity (mydriasis, urinary retention, dry mucous membranes)_
tricyclic antidepressants (TCA) toxicity
32
bradycardia + hypotension + hypoglycaemia within 6 hours of ingestion
beta blocker (BB) overdose beta blocker overdose
33
Severe croup management
nebulised adrenaline (1 mL of 1%
adrenaline solution mixed with 3ml of normal saline)
- observation and repeat dose if needed
34
Burn injury management
– Wash the area with water at room temperature.
– Avoid using ice water as further tissue damage will result otherwise.
– Do not peel the adherent clothing or burning substance.
– Do not apply lotions or creams except hydrogel.
35
Absent/buried P waves + narrow/tall QRS
SVT
36
SVT management
Stable:
1st: Valsalva
2nd: Adenosine
Unstable: DC cardioversion
37
Acute pulmonary oedema management
-Commence oxygen (10–15 L/min via Hudson type mask and reservoir bag).
-Get intravenous access.
-Patient supported in sitting up position.
-Glyceryl trinitrate (vasodilator)
-Continuous positive airway pressure CPAP.
-Intravenous frusemide
– Morphine-to reduce sympathetic nervous activity
38
Acute alcohol withdrawal treatment
Diazepam
39
venlafaxine alternative
- Reboxetine
- mirtazapine
40
MVA + fractured ribs on both sides + paradoxical breathing
Flail chest
41
MVA + fractured ribs of > 2 ribs on one side + paradoxical breathing
Flail chest
42
Flail chest management
Intubation and ventilation
NOTE: Splinting/wrapping considered in the acute setting in the absence of analgesia.
43
Shockable rhythms for defibrillator
- Ventricular tachycardia
- ventricular fibrillation
- asystole
- pulseless cardiac
activity
44
Defib protocol
1. Defib (300j)
2. CPR
3. Defib again + 1mg adrenlaine
4. CPR 2 mins
45
Tall P wave + broad QRS + ST segment depression
Hyperkalaemia
46
Severe hyperkalaemia management
Calcium chloride 10 ml
- reduce risk of ventricular fibrillation
47
most common cause of death seen in pre-hospital STEMI
Ventricular fibrillation
-occur within the first 24h of the onset of symptoms, and of these, over half occur in the first hour
48
Organophosphate poisoning
DUMBELS
–Diarrhoea
–Urination
–Miosis
–Bronchorrhea, bradycardia
–Emesis
–Lacrimation
–Salivation.
49
high-quality CPR
1.The depth of the chest compression should be at least 5 cm.
2.The rate of chest compressions should be 100 per minute and should never be
faster than 120 per minute.
3.The point of compression should be middle of the lower half of the sternum.
4.If the second rescuer is available, they should change the person every 2 minutes or earlier for high-quality CPR.
5.Give 30 compressions followed by two ventilations
50
hypoperfusion + hypotension, + multiorgan dysfunction + white urine
Septic shock
51
Septic shock treatment
- immediate hydration
- broad-spectrum antibiotics,
- possible intubation
- pressors,
- admission to the intensive care unit
52
severe headache, + breathlessness + nausea + vomiting + weakness + lassitude + retinal haemorrhages and venous
tortuosity
Latitude involvement or climbing
acute mountain sickness (AMS)
53
acute mountain sickness (AMS) management
D 🚶⬇️ 🧺 🤢
- Descent
- hyperbaric chambers
- acetazolamide
54
testicular torsion management
Rotate the testes in a medial to lateral direction as if you were opening a book
55
elderly + delirious + blurry vision + dry mouth + constipation
Anticholinergic syndrome
**Why Anticholinergic Syndrome Causes These Symptoms:**
1. **Delirium**:
- Anticholinergic drugs block acetylcholine, a neurotransmitter crucial for memory and cognition, leading to confusion and delirium, especially in the elderly.
2. **Blurry Vision**:
- These drugs cause pupil dilation (mydriasis) and interfere with eye accommodation, resulting in blurry vision.
3. **Dry Mouth**:
- They inhibit salivary gland function, reducing saliva production and causing dry mouth.
4. **Constipation**:
- By decreasing gastrointestinal motility, anticholinergic drugs slow down bowel movements, leading to constipation.
56
Hot and red + Tachycardia + Dry skin
+ Urinary retention + Constipation + Dilation of pupils.
Anticholinergic toxidrome
57
zygomatic bone fracture features
Inability to open the mouth
Periorbital and/or subconjunctival ecchymosis
Horizontal diplopia
Vertical diplopia
Enophthalmos
58
hyperthermia + muscle rigidity + altered mental status + autonomic
instability + antipsychotic medication
Neuroleptic malignant syndrome
59
basophilic stippling + anaemia + low haemoglobin
Lead poisoning
60
Rovsing sign
Acute appendicitis
61
rAUNAUD'S
symmetrical cyanosis of the extremities with persistent, uneven, mottled blue or red discoloration of the skin of the digits, wrists, and ankles, along with profuse sweating and coldness of the fingers and toes
**Raynaud’s phenomenon** (or Raynaud’s disease) is a condition where the blood vessels in certain parts of the body, usually the fingers and toes, temporarily narrow (spasm) in response to cold temperatures or stress. This reduces blood flow to those areas, causing color changes and discomfort.
### What Happens in Raynaud’s?
1. **Trigger**:
- When you’re exposed to cold or sometimes when you’re stressed, the small blood vessels in your fingers and toes tighten up or spasm.
2. **Color Changes**:
- **White**: First, the affected areas may turn white because blood flow is reduced.
- **Blue**: As the blood supply continues to be limited, the areas might turn blue due to lack of oxygen.
- **Red**: When the blood flow returns, the skin might turn red as the vessels reopen, and you might feel tingling or throbbing.
3. **Symptoms**:
- **Cold Fingers or Toes**: The fingers or toes feel very cold and numb during an attack.
- **Pins and Needles**: As blood flow returns, you might feel tingling or throbbing pain.
4. **Why It Happens**:
- The exact cause isn’t always known, but it can be linked to other health conditions, like autoimmune diseases (e.g., lupus, scleroderma), or it might happen on its own (called primary Raynaud’s).
5. **Managing Raynaud’s**:
- **Stay Warm**: Keeping your hands and feet warm can help prevent attacks.
- **Stress Management**: Reducing stress can also help, as stress can trigger symptoms.
- **Medication**: In more severe cases, doctors may prescribe medications to help keep blood vessels open.
### Summary:
**Raynaud’s phenomenon** is a condition where the blood vessels in your fingers and toes temporarily narrow in response to cold or stress, causing them to change color (white, blue, then red) and feel cold or painful. It's generally not dangerous but can be uncomfortable and is managed by keeping warm and reducing stress.
62
Blumberg sign
peritoneal inflammation
- sharp pain when the examiner presses his or her hand over McBurney point and then releases the hand pressure suddenly.
63
increased PaO2 + decreased PaCO2 + increased HCO3
Metabolic alkalosis secondary to bulimia
64
-Blurred vision.
-Dry mouth.
-Unreactive or sluggish reactive pupil.
-Constipation.
-Urinary retention.
-Motor paralysis.
Botulism
65
Hypotension, raised JVP, muffled heart sounds
Beck triad: Cardiac tamponade
66
hypotension with either bradycardia +
normal heart rate despite fluid resuscitation
Neurogenic shock
- give vasopressor
67
previous hx of cardiac disease + bradycardia + hypotension
Cardiogenic shock
- Give dobutamine
68
capillary refill, cool and
mottled peripheries, tachycardia, drowsiness and hypotension
What type of shock?
circulatory shock
69
Blood loss estimation
70
rabies featires
- incubation period varies from 5 days to many years
- fatal encephalitis and brain stem dysfunction
-
71
Rabies management
Thoroughly wash the wound- clean and debride if indicated.
-Transmission between humans has not been proven.
-Post-exposure prophylaxis
72
Rabies Post-exposure prophylaxis regime
first dose of rabies vaccines + immunoglobulins as soon as possible after the exposure. The schedule of vaccinations should be 0, 3, 7 and 14th day
- If immunocompromised: a 5th dose at 28-day post exposure
73
Parkland formula:
(4 x bodyweight x burns %) / 2 (first 8 hours)
74
cleaning fluid intoxication
- potent hepatic toxin
- increased ammonia due to liver damage
- triphasic EEG
75
drooling + radycardia + miosis + increased urination, + diarrhea
organophosphate poisoning
76
