A+E Flashcards

(32 cards)

1
Q

Typical picture of salycilate overdose

A
  • A key concept for the exam is to understand that salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis.
  • Early stimulation of the respiratory centre leads to a respiratory alkalosis
  • Following this, a metabolic acidosis develops along side the respiratory alkalosis due to the direct acid effects of salicylates (combined with acute renal failure).
  • In children metabolic acidosis tends to predominate.

Features
* hyperventilation (centrally stimulates respiration)
* tinnitus
* lethargy
* sweating, pyrexia*
* nausea/vomiting
* hyperglycaemia and hypoglycaemia
* seizures
* coma

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2
Q

treatment of salicylate overdose

A
  • general (ABC, charcoal)
  • urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine
  • haemodialysis

Indications for haemodialysis in salicylate overdose

  • serum concentration > 700mg/L
  • metabolic acidosis resistant to treatment
  • acute renal failure
  • pulmonary oedema
  • seizures
  • coma
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3
Q

child abuse presentations:
- where do they present
- how might they present physically

A

Children may disclose abuse themselves. Other factors which point towards child abuse include:
story inconsistent with injuries
repeated attendances at A&E departments
delayed presentation
child with a frightened, withdrawn appearance - ‘frozen watchfulness’

Possible physical presentations of child abuse include:
bruising
fractures: particularly metaphyseal, posterior rib fractures or multiple fractures at different stages of healing
torn frenulum: e.g. from forcing a bottle into a child’s mouth
burns or scalds
failure to thrive
sexually transmitted infections e.g. Chlamydia, Gonorrhoea, Trichomonas

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4
Q

testicular torsion signs and sx

A
  • pain is usually severe and of sudden onset
  • the pain may be referred to the lower abdomen
  • nausea and vomiting may be present
  • on examination, there is usually a swollen, tender testis retracted upwards. The skin may be reddened
  • cremasteric reflex is lost
  • elevation of the testis does not ease the pain (Prehn’s sign) [positive in epididymitis]
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5
Q

testicular torsion Mx

A

treatment is with urgent surgical exploration
if a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.

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6
Q

acute DKA management

A
  • fluid resus - saline
  • fixed rate insulin [ 0.1 unit/kg/hour] whilst continuing regular injected long-acting insulin but stopping short actin injected insulin [if pt is known diabetic]
  • later add in potassium according to their initial levels on presentation
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7
Q

DKA diagnostic criteria

A

glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

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8
Q

DKA resolution is defined as:

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

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9
Q

what extra care should children and young adults get after treatment for DKA

A

they are at greater risk of cerebral oedema t4
1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought

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10
Q

Complications may occur from DKA itself or the treatment:

A
  • gastric stasis
  • thromboembolism
  • arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  • acute respiratory distress syndrome
  • acute kidney injury
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11
Q

a child presents to A+E with no signs of life - how do you proceed

A

5 rescue breaths then 15 chest compressions to every 2 ventilation breaths

  • For a child under 1, the two-thumb encircling or two-finger techniques should be used.
  • For a small child, the one-handed technique should be used.
  • For a larger child, the two-handed technique can be used (as for adults).
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12
Q

define hypothermia

A

unintentional reduction of core body temperature below the normal physiological limits

  • Mild hypothermia: 32-35°C
  • Moderate or severe hypothermia: < 32°C
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13
Q

hypothermia risk factors

A

Risk factors:

  • General anaesthesia
  • Substance abuse
  • Hypothyroidism
  • Impaired mental status
  • Homelessness
  • Extremes of age
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14
Q

Signs of hypothermia include:

A
  • shivering
  • cold and pale skin. Frostbite occurs when the skin and subcutaneous tissue freeze, causing damage to cells.
  • slurred speech
  • tachypnoea, tachycardia and hypertension (if mild)
  • respiratory depression, bradycardia and hypotension (if moderate)
  • confusion/ impaired mental state
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15
Q

ECG signs of hypothermia

A

As the core temperature approaches 32°C to 33°C, acute ST-elevation and J waves or Osborn waves may appear

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16
Q

hypothermia investigations

A
  • Temperature. Special low-reading rectal thermometers or thermistor probes are preferred for measuring core body temperature. The patient’s temperature should be tracked over time, to check for improvement.
  • 12 lead ECG. As the core temperature approaches 32°C to 33°C, acute ST-elevation and J waves or Osborn waves may appear
  • FBC, serum electrolytes. Haemoglobin and haematocrit can be elevated (due to haemoconcentration). Platelets and WBCs are low due to sequestration in the spleen. Monitoring potassium is advised as hypothermic patients can be hypokalaemic due to a shift of potassium into the intracellular space.
  • Blood glucose. Stress hormones are increased, and the body can have more peripheral resistance to insulin.
  • Arterial blood gas
  • Coagulation factors
  • Chest X-ray
17
Q

T/F
rapid rewarming is the best treatment option for hypothermic pts

A

FALSE
this can lead to peripheral vasodilation and shock

18
Q

who should be treated with acetylcysteine in paracetmol OD

A
  • the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
  • there is a staggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or
  • patients who present 8-24 hours after ingestion of an acute overdose of more than 150 mg/kg of paracetamol even if the plasma-paracetamol concentration is not yet available
  • patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
    • acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated whilst seeking specialist advice
19
Q

how is acetylcysteine administered + why

A

IV infusion over 1 hour as it can cause anaphylactic reactions when given over shorter periods

20
Q

management of PE

A

HAEMODYNAMICALLY STABLE PTs

  • DOACs first line for most people, including cancer patients. [apixaban or rivaroxiban]
    • 2nd line = LMWH –> dabigatran or edoxaban or warfarin.
  • low risk patients are managed as outpatients and higher risk are admitted.
  • PE severity index score [PESI] is used to determine risk.
  • anti-coagulate for at least 3 months [provoked PE’s]
    • treat for 3 extra months for unprovoked PEs and active cancer pts.

HAEMODYNAMICALLY UNSTABLE PTs

  • thrombolyse.
  • massive PE presents with haemodynamic instability, particularly hypotension.
21
Q

Well’s score features

A

Clinical probability simplified score
DVT likely: 2 points or more
DVT unlikely: 1 point or less

22
Q

DVT Mx based on wells score

23
Q

signs of a PE on ECG

A

S1 Q3 T3

  • a prominent S wave in lead I, a Q wave in lead III, and a T wave inversion in lead III
  • indicates right heart strain which is associated with PE
    • can be seen in other conditions causing right ventricular strain, such as acute bronchospasm, pneumothorax, and other acute lung disorders t4 NOT specific
    • not always seen in PE t4 not sensitive
  • used alongside clinical features
24
Q

what are the 3 determining factors for how you approach AF management

A
  1. haemodynamic in/stability
  • unstable pts are electrically cardioverted
  • stable pts, see below.
  1. how acute the AF is:
  • <48 hours; give rhythm control
  • > 48 hours OR uncertain time frame; give rate control
  1. anticoagulation - all pts require anticoagulation usually with a DOAC [1st line] or warfarin [2nd line]
25
which AF pts receive rate control as treatment
all pts except: * A reversible cause for their AF * New onset atrial fibrillation (within the last 48 hours) * Heart failure caused by atrial fibrillation * Symptoms despite being effectively rate controlled
26
which AF pts receive rhythm control as treatment
* A reversible cause for their AF * New onset atrial fibrillation (within the last 48 hours) * Heart failure caused by atrial fibrillation * Symptoms despite being effectively rate controlled
27
rate control options in AF
Rate control aims to get the heart rate below 100 and extend the time during diastole for the ventricles to fill with blood. 1. Beta blocker first-line (e.g., atenolol or bisoprolol) 2. Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure) 3. Digoxin - NOT 1st line(only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity, may be useful in coexistent HF)
28
Rhythm control options in AF
Rhythm control aims to return the patient to normal sinus rhythm. This can be achieved through: - Cardioversion - electrical or pharmacological - electrical is done with a defibrilator and can be done immediately or after 3 weeks of anticoagulation if the pt is stable. always done under sedation or GA - pharmacological cardioversion is done with **Flecainide** or **Amiodarone** (the drug of choice in patients with structural heart disease) - immediate or delayed - done immediately if the AF is new onset and present for <48 hours OR if pt is lifethreatening haemodynamically unstable. - delayed can be used if the atrial fibrillation has been present for more than 48 hours and they are stable - Long-term rhythm control using medications
29
AF treatment option for pts that don't respond to rate or rhythm drug treatment
Catheter ablation: burning areas of abnormal electrical activity. Used when drug treatment for rate or rhythm control is not adequate or tolerated, there are two options for ablation: - Left atrial ablation - AV node ablation + pace maker all pts must be anti-coagulated before hand Anticoagulation afterwards depends on CHADsVASc score
30
what are the 4H's and 4T's
reversible causes of cardiac arrest
31
reversible causes of cardiac arrest
4H's and 4T's - 4 hypo's
32