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Finals > Acute Care > Flashcards

Acute Care Flashcards

1
Q

What are the causes of airway obstruction

A

central nervous system depression
swelling - infection or anaphylaxis
foreign body
bronchospasm

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2
Q

What can cause central nervous system depression

A 
head injury
intracerebral bleed
hypercapnia
hypoglycaemia
alcohol
opioids
general anaesthetic
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3
Q

What can cause respiratory arrest

A

decreased respiratory drive (due to CNS depression)
decreased resp effort
lung disorders

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4
Q

What is the treatment for ACS

A

IV morphine + antiemetic
15L oxygen via non-rebreathe mask if sats <94%
sublingual glyceryl nitrate (unless hypotensive)
Aspirin 300mg crushed/chewed

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5
Q

How is A assessed

A

speak to patient
listen to breathing sounds
look at breathing pattern

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6
Q

How is airway obstruction treated

A

15L oxygen via non-rebreathe mask
airway manoeuvres
suction
Guedel/nasopharyngeal

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7
Q

How is B assessed

A 
resp rate
o2 sats
pattern of breathing
chest deformity
trachea
chest expansion
percussion
breath sounds - ?rattle, wheeze, stridor
auscultate
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8
Q

How is C assessed

A 
hands - ?cool, warm, pale, pink, mottled
CRT
peripheral and central pulses
HR
BP - wide PP = arterial vasodilation, narrow PP = arterial vasoconstriction
auscultate
ECG
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9
Q

How is D assessed

A

AVPU
check drug chart for drugs that cause reduced consciousness
pupils
blood glucose

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10
Q

Which cardiac arrest rhythms are shockable?

A

VF

pulseless VT

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11
Q

Which cardiac arrest rhythms are non-shockable?

A

asystole

PEA

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12
Q

describe the treatment of shockable cardiac arrest

A

CPR
secure airway
break CPR every 2 mins to assess rhythm
give shock 150J first
repeat
after third shock give 300mg amiodarone IV and adrenaline 1mg IV
continue CPR and checks every 2mins
repeat 1mg adrenaline IV at alternate shocks
can give 150mg amiodarone IV after five shocks

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13
Q

describe the treatment of non-shockable cardiac arrest

A

CPR
adrenaline 1mg IV STAT
check rhythm every 2 mins
give 1mg adrenaline IV every other cycle

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14
Q

State the reversible causes of cardiac arrest

A

Hypoxia
Hyperkalaemia, hypokalaemia, hypoglycaemia
Hypovolaemia
Hypothermia

Thrombosis - MI/PE
Tension pneumothorax
Tamponade
Toxins

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15
Q

State the steps in management of bradycardia

A

if signs of adverse features, give atropine 500mcg IV
if unsuccessful, arrange senior help and transvenous pacing

if no adverse features, assess for risk of asystole

if risk of asystole, ger senior help and arrange transvenous pacing

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16
Q

What are the adverse features in tachy/bradycardia

A

shock
heart failure
syncope
MI

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17
Q

What are the steps in management of broad complex tachycardia

A

are there adverse features present?

no

  • correct electrolyte abnormalities
  • if most likely monomorphic VT give amiodarone 300mg IV over 20 mins
  • if polymorphic VT give 2g magnesium sulfate IV over 10mins

yes - call for senior help, sedate and cardiovert. give 300mg amiodarone IV over 20 mins
900mg amiodarone IV via central line over 24h

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18
Q

What is the difference between monomorphic and polymorphic VT

A

mono - caused by structural abnormalities. not likely to convert into VF

poly - caused by electrolyte abnormalities, likely to convert into VF

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19
Q

What are the steps in management of narrow complex tachycardia

A

vagal maneouvres
IV adenosine 6mg, 12mg, 12mg

adverse features?

yes

  • sedation and cardioversion
  • amiodarone 300mg IV over 20 mins then 900mg amiodarone IV via central line over 24h

no - beta blocker eg. IV metoprolol, amiodarone 300mg IV over 1h or digoxin

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20
Q

How is GCS calculated?

A 
Eye Opening	
Spontaneous	4
To sound	3
To pressure	2
None	1
Verbal Response	
Orientated	5
Confused	4
Words	3
Sounds	2
None	1
Motor Response	
Obeys commands	6
Localise to pain	5
Withdraws from pain	4
Flexor response	3 (decorticate)
Extensor response	2 (decerebrate)
None	1
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21
Q

What are the common causes of reduced GCS

A 
metabolic:
drugs
sepsis
hypoglycaemia/hyperglycaemia
respiratory acidosis
hypoxia
hypothermia
addisonian crisis
hepatic or uraemic encephalopathy
neurological:
trauma
meningitis/encephalitis
tumour
stroke, 
SAH
epilepsy
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22
Q

What are the key signs and symptoms of anaphylaxis

A 
Onset within minutes
Airway and breathing
Dyspnoea, respiratory distress, wheeze, stridor
Cyanosis
Circulation
Tachycardia, hypotension
Skin
Urticaria, angioedema
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23
Q

Describe the pathophysiology of anaphylaxis

A

Sensitisation phase:
Immune system encounters allergen and makes immunoglobulin E (IgE) against it
No clinical features occur

Effector phase:
Allergen cross-links IgE on surface of mast cells
widespread degranulation and release of histamine
mediates inflammatory bronchospasm, vasodilatation, increased capillary permeability, and tissue oedema

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24
Q

What dose of adrenaline do you give to an adult in anaphylaxis

A

0.5mg (0.5 ml of 1:1,000) IM

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25
Q

What dose of adrenaline do you give to a child 6-12 years in anaphylaxis

A

300 micrograms (0.3 ml of 1:1,000) IM

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26
Q

What dose of adrenaline do you give to a child aged 5 and under in anaphylaxis

A

150 micrograms (0.15 ml of 1:1,000) IM

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27
Q

What drugs apart from adrenaline do you give in anaphylaxis

A

chlorphenamine 10mg IV
hydrocortisone 200mg IV

can give salbutamol 5mg neb and ipatropium bromide 0.5mg neb if wheeze

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28
Q

What blood test can help in the retrospective diagnosis of anaphylaxis

A

Mast cell tryptase
Take three samples taken as soon as possible, after 1-2 hours and after 24 hours
Useful in making a retrospective diagnosis but the absence of a rise does not exclude anaphylaxis

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29
Q

What are the steps in management of anaphylaxis

A 
SENIOR HELP
secure airway
15L oxygen non rebreate mask
adrenaline 0.5mg (0.5ml 1:1000) IM
IV access - 2x wide bore cannulae
500ml 0.9% sodium chloride over 15mins
10mg chlorphenamine and 200mg hydrocortisone IV
nebs if wheeze
referral suing SBAR
admit
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30
Q

What is the ongoing management for a patient after anaphylaxis

A

medicalert bracelet

epipen x2

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31
Q

How is adrenaline administered IM

A

into anterolateral aspect of middle third of thigh

“blue to sky, orange to thigh”

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32
Q

State the initial management of an NSTEMI

A

oxygen if sats low
morphine 5-10mg IV and metoclopramide 10mg IV
sublignual GTN
aspirin 300mg + second antiplatelet
Metoprolol or verapamil or diltiazem - rate control
ACEi
Fondaparinux - anticoagulation
calculate GRACE score ?PCI within 72 hours

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33
Q

What investigations should be done in suspected pulmonary oedema?

A

ECG
U+E, troponin, ABG
CXR
echo

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34
Q

What are the possible causes of pulmonary oedema

A

heart failure due to MI, valvular heart diseae, arrhythmias
ARDS
fluid overload
neurogenic

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35
Q

What are the signs of heart failure on CXR

A 
alveolar oedema (bat's wings)
kerley B lines
Cardiomegaly
upper lobe diversion
pleural effusion
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36
Q

What is the immediate management of severe pulmonary oedema

A

A
B - 15L oxygen via non-rebreathe, listen to chest
C - ECG, IV access

IV diamorphine 1.35-5mg slowly
IV furosemide 40mg slowly
2 puffs GTN spray if BP >90 systolic

SENIOR HELP
?CPAP, nitrate infusion

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37
Q

What are some causes of cardiogenic shock

A 
MI
arrythmias
myocarditis
valve destruction
cardiac tamponade
aortic dissection
PE
tension pneumothorax
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38
Q

What is the immediate management of cardiogenic shock

A

15L oxygen via non-rebreathe
1.25-5mg diamorphine IV for pain and anxiety

SENIOR HELP

ECG
FBC, U+E. troponin, ABG
CXR, echo

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39
Q

What are the signs of a life-threatening asthma attack?

A 
PEFR <33% best
silent chest, cyanosis, feeble respiratory effort
slow HR, low BP
exhaustion, confusion, coma
ABG - reduced pO2, pH <7.35
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40
Q

What are the signs of a near fatal asthma attack

A

rise in pCO2

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41
Q

What are the signs of a severe asthma attack

A

PEFR <50% best
HR >110
RR >25
unable to complete sentences

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42
Q

What are the steps in management of severe or life threatening asthma

A

salbutamol 5mg NEB over 15mins
ipatropium bromide 0.5mg NEB over 15 mins
hydrocortisone 100mg IV or prednisolone 40mg PO

if life threatening:
SENIOR HELP, ICU
monitor ECG
magnesium sulfate 2g IV over 20mins

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43
Q

What is the ongioing management of a severe asthma attack

A

admission
nebulised salbutamol every 4 hours
prednisolone 40-50mg PO OD for 5-7days

for discharge;
stable for 24 hours on discharge meds
inhalers x2 prescribed
peak flow >75% best/predicted

see GP within 1 week
resp clinic within 4 weeks

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44
Q

What is the immediate management for IECOPD

A

salbutamol 5mg NEB over 4h
ipatropium bromide 0.5mg NEB over 6h

CXR, ABG

controlled oxygen therapy

200mg hydrocortisone IV + 30mg prednisolone PO OD for 7 days

Abx if infection - doxycycline

if no respomse: NIPPV, intubation and ventilation,

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45
Q

What investigations should be done in IECOPD

A

ECG
FBC, CRP, U+E, ABG,
blood cultures, sputum culture
CXR

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46
Q

How do you aspirate a pneumothorax?

A

16-18G cannula
2nd ICS
mid clavicular line

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47
Q

What are the most common organisms to cause CAP

A

streptococcus pneumoniae
haemophilus influenzae
mycoplasma pneumoniae

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48
Q

How is the severity of CAP assessed?

A

CURB-65

confusion
urea >7mmol/l
RR >30
BP <90/60
>65y
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49
Q

How is the management of CAP changed depending on the CURB-65 score

A

0-1 = 5 days 1g/8h amoxicillin at home
2 = 7-10days of co-amoxicav 1.2g/8g IV + clarithromycin 500mg/12h IV in hospital
3 or more = ICU referral

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50
Q

Describe the management of PE

A

15L oxygen via non-rebreathe if hypoxic
IV access
morphine 5-10mg IV + metoclopramide 10mg IV
LMWH or fondaparinux IV

NB: if massive PE, give immediate 50mg alteplase bolus not LMWH

if BP <90 systolic:
IV fluids, then SENIOR HELP for dobutamine, then noradrenaline

if BP >90 systolic, start warfarin

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51
Q

What investigations should be carried out in PE

A

ECG
FBC, U+E, clotting, ABG, ?d-dimer
CXR, CTPA

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52
Q

What are the causes of upper GI bleed

A 
PUD
mallory-weiss tears
oesophageal varices
oesophagitis
malignancy
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53
Q

What is the immediate management of an upper GI bleed

A

protect airway
NBM
2x cannula
bloods - FBC, LFT, U+E, glucose, clotting, G+S, cross-match
IV fluids
if grade III or IV shock give blood
correct clotting abnormalities - Vit K, FFP

?ICU/HDU

endoscopy- - within 4hrs for varices. 12-24h if unstable on admission

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54
Q

What medications should be given in acute variceal bleeding

A

terlipressin

omeprazole - prevents stress ulceration

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55
Q

What score can be used to assess prognosis in acute GI bleeds

A

Rockall score

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56
Q

What medication can be given pre-hospital in suspected meningitis

A

1.2g benzylpenicillin IM

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57
Q

What is Kernig’s sign

A

pain and resitance on passive extension of knee with flexed hip

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58
Q

What is the immediate management for meningitis

A

IV fluids
IV cefotaxime 2g (+amoxicillin if <3m or >55y)

if septicaemic - do not attempt LP, contact ITU if shock

if meningitic - dexamethasone 4-10mg/6h IV, LP if no shock and no raised ICP

contact tracing and prophylaxis
inform public health

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59
Q

What are the most common causitive organisms for meningitis?

A

6-60y = Neisseria meningitidis, Streptococcus pneumoniae

<3m = Group B strep,, E coli, Listeria monocytogenes

> 60y/immunocompromised = Listeria monocytogenes

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60
Q

What investigations should be done in meningitis

A

urine dip
FBC, U+E, LFT, clotting, glucose, VBG, ABG
blood cultures
CSF MC&S, gram stain, protein,glucose, virology, lactate
?CT head

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61
Q

What is the typical presentation of encephalitis

A

odd behaviours
reduced consciousness
focal neurology - aphasia
seizure

preceded by infectious prodrome - raised temp, rash, lymph, conjunctivitis

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62
Q

What is the differential diagnosis for encephalitis

A 
hypoglycaemia
uraemic encephalopathy
hepatic encephalopathy
DKA
drugs
SLE
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63
Q

What organisms can cause encephalitis

A

viral - HSV, CMV, EBV, VZV, HIV
bacterial - any bacterial meningitis, TB, malaria
aspergillus

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64
Q

What investigations should be done in encephalitis

A

FBC, U+E,
blood cultures, serum PCR
CT with contrast/MRI
LP

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65
Q

What is the treatment for encephalitis

A

IV aciclovir
supportive therapy in ICU/HDU
phenytoin for seizures

66
Q

define status epilepticus

A

seizure for >30mins

repeated seizures without regaining consciousness

67
Q

What is the immediate management of status epilepticus

A

secure airway - oral/nasal, intubate
recovery position
remove false teeth

15L oxygen via non-rebreathe

IV access 
slow IV bolus lorazepam 2-4mg
thiamine if alcoholism or malnourishment
suspected
IV dextrose if hypoglycaemic
IV fluids if hypotension

if seizure continues, give phenytoin or daizepam. then general anaesthesia

68
Q

What features are seen in prolonged seizures

A

raised HR
HTN
raised glucose
lactic acidosis

69
Q

What investigations are useful in status epilepticus

A 
BM, o2 sats!!!
FBC, U+E, LFT, glucose, calcium, toxicology, anticonvulsant levels, ABG/VBG
blood cultures
CT head 
LP
70
Q

How is lactic acidosis treated in status epilepticus

A

resolves spontaneously!

non need for sodium bicarbonate

71
Q

What are the signs of a basal skull fracture

A

haemotympanum
panda eyes
CSF leak through ears/nose
Battle’s sign

72
Q

State the criteria for a CT head in a head injury of an adult

A

within 1 hour:
Glasgow Coma Scale (GCS) <13 when first assessed or GCS <15 two hours after injury
Suspected open or depressed skull fracture
Signs of base of skull fracture
Post-traumatic seizure
Focal neurological deficit
>1 episode of vomiting

within 8 hours of injury:
coagulopathy or on oral anticoagulant

73
Q

What investigations should be done in head injury>

A

GCS,
FBC, U+E, glucose, alcohol, clotting, toxicology
ABG
CT head if indicated
cervical xray if tenderness or deformity posteriorly

74
Q

State the management of hyperkalaemia

A

ECG for signs
10ml 10% calcium gluconate IV - stabilise cardiac membrane
10 units actrapid in 50ml 20% glucose

75
Q

What are the signs of hyperkalaemia on ECG

A

tall tented T waves
flat p waves
increased PR interval

76
Q

Which drugs can give dilated pupils

A

amphetamines
cocaine
TCA

77
Q

Which drugs can give metabolic acidosis

A

alcohol
methanol
paracetamol
Carbon monoxide

78
Q

What effects can salicylate OD cause

A

hypoglycaemia

renal impairment

79
Q

Which drugs class as salicylates

A

aspirin

80
Q

What are the features of delerium

A

acute onset
transient and reversible satet of confusion
result of organic process

81
Q

Describe the CAM diagnostic tool for delerium

A

1 + 2 + 3/4 = delerium

  1. acute onset, fluctuation
  2. 20-1 inattention
  3. disorganised thinking
  4. alteration of consciousness
82
Q

state some causes of acute confusional state

A 
stroke
meningitis/encephalitis
hepatic/uraemic encephalopathy
hypoglycaemia
hyponatraemia
hypo/hyperthyroid
b12/thiamine
MI
pneumonia
constipation
UTI
medications
drugs - alcohol/recreational
83
Q

What investigations need to be done in acute confusional state

A

ECG, urine dip, PR
FBC, U+E. CRP, LFTs, TFT, B12, folate, trop, glucose
blood cultures, urine culture, sputum culture
CXR, CT if focal neurology

84
Q

What drugs can be given to sedate a patient

A

haloperidol 0.5mg IM/oral

lorazepam 2mg IV/IM

85
Q

What is seizure like activity during a vasovagal faint called

A

reflex anoxic convulsion

86
Q

Describe the layers of the meninges

A 
SKULL
extradural/epidural space
dura mater
subdural space
arachnoid mater
subarachnoid space
pia mater
BRAIN
87
Q

What is an extradural/epidural haematoma and what causes it

A

collection of blood in the extradural space between the skull and the dura mater

can be due to fractured temporal or parietal bone damaging the middle meningeal artery or vein.
can also be due to tear in dural venous sinuses

88
Q

What are the features of an extradural haematoma

A 
history of head injury leading to LOC
lucid interval
then deterioration of conscious level
headache
N+V
seizures
skull fracture
bradycardia, HTN
haematoma over fracture
CSF leakage
reduced GCS
unequal pupils - fixed and dilated due to compression of CNIII 
focal neurology
89
Q

Explain Cushing’s reflex

A

raised ICP
increase in systemic BP to try to maintain perfusion to brain
caroitid baroceptors recognise rise in BP and decrease HR in response

HTN, low HR

90
Q

What investigations should be done in extradural haematoma

A

baseline FBC, U+E
xray skull and spine
CT scan - repeat if further deterioration

91
Q

How does an extradural haematoma appear on CT

A

biconvex hyperdense abnormality

midline shift

92
Q

How is an extradural haematoma managed

A

A-E
if RICP - IV hypertonic saline or mannitol
burr hole
craniotomy and evacuation

93
Q

What is a subdural haematoma

A

collection fo blood in the subdural space between dura mater and arachnoid mater

94
Q

What is the difference between an acute, subacute and chronic subdural haematoma

A

subacute - 3-7d after injury. clotted blood liquefies

chronic - 2-3 weeks after injury. blood becomes serous fluid

95
Q

What is the difference between a simple and complicated subdural haematoma

A

simple = no parenchymal injury

complicated = associated underlying parenchymal injury eg. contusion

96
Q

Where can the blood causing a subdural haematoma come from

A

bridging veins - tear

cortical arteries (branches of carotids)

97
Q

Which groups of people are subdural haematomas more common in and why

A

infants - immature veins - tear. NAI

elderly - cerebral atrophy. tension on bridging veins

alcoholics - cerebral atrophy and less platelets and increased bleeding time

anticoagulation

98
Q

What are the features of subdural haematoma

A

acute: LOC

chronic: gradually progressive
anorexia
N+V
neurological deficit
progressive headache
reduced GCS
bradycardia and HTN
papilloedema
(raised fontanellesi in infant)
99
Q

Give some differentials for a subdural haematoma

A 
other intracranial bleed
meningitis or encephalitis
cerebral tumour
stroke
metabolic causes of confusion and reduced consciousness - DKA, hepatic encephalopathy
decompensation of dementia
100
Q

What differentials should be done for subdural haematoma

A

FBC, U+E, VBG, LFT, clotting, G+S, cross match
blood culture
CT head
cervical spine xray/CT if severe trauma

101
Q

What is seen on CT in subdural haematoma

A

crescenteric collection

hyperdense - white, acute

hypodense - black, chronic

102
Q

What is the management of subdural haematoma

A

A-E
if RICP - IV hypertonic saline or mannitol
burr hole

if acute and asymptomatic - can monotor obs and examination, do serial CTs

if large, focal signs, RICP, midline shift - needs emergency craniotomy and clot evacuation

103
Q

What causes a subarachnoid haemorrhage

A

usually due to bleed from berry aneurysm in circle of willis

or trauma

104
Q

What are the risk factors for developing berry aneurysms

A 
HTN
smoking
cocaine
alcohol
genetics
Marfan's
FH - first degree relative
105
Q

What are the features of a subarachnoid haemorrhage

A 
sudden explosive headache - diffuse, severe, pulsates towards occiput
seizure
confusional state
neck stiffness
photophobia

in past few weeks - headache, dizziness, orbital pain, diploplia

reduced consciousness
intraocular haemorrhage
isolated dilated pupil with loss of light reflex - die to brain herniation
focal neurology

106
Q

Give some differentials for SAH

A 
stroke
meningitis
trauma
primary sexual headache
carotid artery dissection
hypertensive emergency
107
Q

How should SAH be investigated

A

immediate CT head without contrast
LP if CT inconclusive
angiography to identify origin of bleed

108
Q

What can be seen on CT in SAH

A

hyperdense in basal cisterns and sulci

109
Q

What can be found on LP in SAH

A

xanthochromia

= yellow discolouration due to presence of bilirubin from RBC breakdown

110
Q

How is SAH managed

A

A-E
transfer to neuro unit with ITU
prevention of vasospam - nimodipine
prevent rebleeding - clipping or coiling

111
Q

What is the difference between clipping and coiling for SAH

A

clipping - craniotomy, clips placed around neck of aneurysm

coiling - femoral catheterisation, platinum coil to obliterate aneurysm and for clot within it

112
Q

What is meningitis?

A

inflammation of the meninges

can be infective or non-infective

113
Q

What is meningococcal disease

A

meningococcal meningitis, meningococcal septicaemia, or a combination of both.

caused by Neisseria meningitidis

114
Q

Which bacteria most commonly cause meningitis in neonates

A

Streptococcus agalactiae,
Escherichia coli,
S. pneumoniae,
Listeria monocytogenes

115
Q

Which bacteria most commonly cause meningitis in children and young people

A

Neisseria meningitidis,
Streptococcus pneumoniae,
Haemophilus influenzae type b (Hib)

116
Q

Which bacteria most commonly cause meningitis in the elderly and immunocompromised

A

Streptococcus pneumoniae
Listeria monocytogenes
TB
gram -ve organisms

117
Q

What are risk factors for meningitis

A 
Young age
Winter season 
An absent or non-functioning spleen.
Older age (more than 65 years).
Immunocompromised state
Organ dysfunction
Smoking, including passive smoking.
Living in overcrowded households or in military barracks.
CSF or dural shunt
sickle cell disease
118
Q

What are risk factors for meningitis in neonates

A 
low birth weight (below 2500 g), 
premature delivery, 
premature rupture of membranes, 
traumatic delivery, 
fetal hypoxia 
maternal peripartum infection.
119
Q

What can cause aseptic meningitis

A 
partially treated bacterial meningitis.
Viral infection - eg, mumps, echovirus, Coxsackievirus, HSV and herpes zoster virus, HIV, measles, influenza, arboviruses
Fungal infection
Parasites
atypical TB, syphilis, Lyme disease,
Kawasaki disease.
120
Q

What can cause non-infective meningitis

A

Malignant cells (leukaemia, lymphoma, other tumours).
Chemical meningitis (intrathecal drugs, contaminants).
Drugs (non-steroidal anti-inflammatory drugs (NSAIDS), trimethoprim).
Sarcoidosis.
Systemic lupus erythematosus.
Behçet’s disease.

121
Q

What are the symptoms and signs of meningococcal disease

A

Non-blanching rash.
Stiff neck.
Capillary refill time of more than 2 seconds, cold hands and feet.
Unusual skin colour.
Shock and hypotension.
Leg pain.
Back rigidity.
Bulging fontanelle.
Photophobia.
Kernig’s sign (person unable to fully extend at the knee when hip is flexed).
Brudzinski’s sign (person’s knees and hips flex when neck is flexed).
Unconsciousness or toxic/moribund state.
Paresis.
Seizures.
Focal neurological deficit including cranial nerve involvement and abnormal pupils.

also: 
Fever.
Vomiting/nausea.
Lethargy.
Irritability/unsettled behaviour.
Ill appearance.
Refusing food/drink.
Headache.
Muscle ache/joint pain.
Respiratory symptoms/signs or breathing difficulty.
122
Q

What is Kernig’s sign

A

with hips flexed, passive knee extension leads to pain and resistance

sign of meningitis

123
Q

What is Brudzinski’s sign?

A

if their head is bent forwards, the hips flex

sign of meningitis

124
Q

Describe the rash that could be seen in meningococcal meningitis

A

at first: generalised petechial rash - red/purple non blanching macules <2mm

then: purple purpuric rash, >2mm

125
Q

What investigations need to be done in suspected meningitis

A

LP - Gram stain, Ziehl-Neelsen stain (TB), cytology, virology, glucose, protein, culture, rapid antigen screen or polymerase chain reaction (PCR) if available and India ink for cryptococci

FBC, U+E, CRP, coaf, VBG
blood culture

126
Q

What might contraindicate an LP in meningitis

A

raised intracranial pressure (reduced consciousness, very bad headache, frequent fits)
or focal neurology.

127
Q

How is suspected meningitis managed in the communirty

A

999 for admission

STAT dose of benzylpenicillin

128
Q

Which antibiotics are used to treat meningitis empiraclly

A

<3m - IV cefotaxime + amoxicillin or ampicillin

>3m - IV ceftriaxone

129
Q

Which antibiotics are used to treat meningococcal meningitis

A

IV ceftriaxone

130
Q

Which antibiotics are used to treat pneumococcal meningitis

A

vancomycin + cefotaxime or ceftriaxone

131
Q

Which antibiotics are used to treat meningitis caused by Hib

A

ceftriaxone

132
Q

How is viral meningitis treated

A

supportive management
corticosteroids - reduces risk of hearing loss and long lasting neuro complications
aciclovir if herpetic
ganciclovir if CMV

133
Q

When might you suspect viral over bacterial meningitis

A

features may be more mild and complications (eg, focal neurological deficits) less frequent.

Any person presenting with suspected meningitis should therefore be managed as having bacterial meningitis until proved otherwise!!!

134
Q

How are close contacts treated in meningitis

A

if it was meningococcal meningitis, close contacts need ciprofloxacin or rifampicin as prophylaxis

135
Q

When are people vaccinated against meningitis

A

2,4,12m - meningitis B

17-18y - meningitis ACWY

136
Q

Give some complications of meningitis

A

Immediate:
septic shock,
DIC
coma with loss of protective airway reflexes,
cerebral oedema and raised intracranial pressure,
septic arthritis,
Subdural effusions
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Seizures

Delayed: 
decreased hearing, or deafness; 
multiple seizures, 
focal paralysis, 
subdural effusions, 
hydrocephalus, 
intellectual deficits, 
ataxia, 
blindness, 
Waterhouse-Friderichsen syndrome - adrenal gland failure due to bleeding into the adrenal glands
peripheral gangrene.
137
Q

What are the gram stain results of Streptococcus pneumoniae

A

gram positive diplococci/chain

138
Q

What are the gram stain results of Escherichia coli

A

gram negative bacilli

139
Q

What are the gram stain results of Haemophilus influenzae

A

gram negative coccobacilli

140
Q

What are the gram stain results of Listeria monocytogenes

A

gram positive rod

141
Q

What is a burn

A

injury caused by exposure to thermal, chemical, electrical or radiation energy

142
Q

What is a scald? What depth burn does it cause

A

a burn caused by contact with a hot liquid or steam

superficial or superficial dermal

143
Q

What is the difference between a complex and a non-complex burn

A

non-complex:
partial thickness burn affecting <15% TBSA (10 in children, 5 in <1yr)
deep partial thickness <1% TBSA
not affecting critical area

complex:
partial thickness burn affecting >15% TBSA (10 in children, 5 in <1yr)
affects critical area
chemical or electrical

144
Q

What is a critical body area in a burn

A

face, hands, feet, perineum, or genitalia; burns crossing joints, and circumferential burns.

145
Q

Describe a superficial epidermal burn

A

only affects epidermis, does nto reach dermis
red and painful skin
no blistering
blanching on CR, <2secs

146
Q

Describe a partial thickness superficial dermal burn

A

affects epidermis and upper dermis
red/pale pink
painful blistering
blanches on CR, >2secs

147
Q

Describe a partial thickness deep dermal burn

A 
affects epidermis and upper and deep dermis. NOT subcutaneous tissues
dry blotchy red skin
blistering
CR does not blanch
painful
148
Q

Describe a full thickness burn

A

through all layers of skin to subcutaenous tissue, can reach muscle or bone
white, brown, black skin. dru, leathery, eaxy
no blisters
does not blanch on CR
painless

149
Q

How is the total body surface area affected from a burn calculated

A

Wallace’s rule of Nine’s

Lund and Browder chart - more accurate

150
Q

How do you calculate TBSA using Wallace’s rule of 9’s

A 
head - 9%
anterior trunk - 18%
posterior trunk - 18%
arm - 9%
leg - 9%
151
Q

What investigations need to be done in a burn

A

FBC, U+E, G+S, crossmatch, carboxyhaemaglobin,
CXR
cardiac monitoring

152
Q

How is a minor burn managed

A

rinse with cold tap water for at least 20 minutes
if blisters >1cm, can be aspirated using aseptic technique
non-adhesive dressing with gauze padding - change every 3-5 days
reassess at 48 hours
? tetanus prophylaxis

153
Q

How is a major burn managed

A

A - any inhalation injury? If yes, intubation!!

B - high flow o2 if risk of CO poisioning

C - two large bore cannulae. Fluids (Hartmann’s) if >15% full/partial thickness burns (10% in children)

154
Q

How is the amount of fluid resuscitation needed for a burn calculated

A

Parkland’s formula

4ml x weight in kg X %TBSA affected

Half given over 8 hours, rest given over next 16 hours

155
Q

When might a patient need to be referred to a burns unit?

A

All complex burn
full thickness burns
Deep dermal burns affecting more than 5% of total body surface area in adults, and all deep dermal burns in children.
All chemical and electrical burns (including lightning injuries).
Any high-pressure steam injury.
NAI
Burns affecting critical area
Circumferential deep dermal burns in any age group.
Burns associated with suspected inhalation injury.
Burns associated with co-morbidities that may affect wound healing or increase the risk of complications.
Burns associated with significant other injuries or trauma (such as crush injuries, fractures, head injury, or penetrating injuries).
Burns associated with sepsis.
Children under 10 years of age, or adults over 49 years of age.

156
Q

How might a circumferential burn to the torso or limb need to be managed?

A

Escharotomy
= division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the torso), or relieve compartment syndrome and oedema (where a limb is involved)

157
Q

What is the antidote in a benzodiazepine overdose

A

Flumazenil (for respiratory arrest) 200mcg over 15 IV

then 100mcg at 60s intervals if needed.

158
Q

What are the features of salicyclate toxicity

A

Vomiting, dehydration, hyperventilation, tinnitus, vertigo, sweating.

respiratory alkalosis due to a direct stimulation of the central respiratory centres and then develop a metabolic acidosis.

159
Q

What arethe features of paracetamol overdose

A

None initially, or vomiting ± ruq pain.

Later: jaundice and encephalopathy from liver damage (the main danger) ± acute kidney injury (aki).

160
Q

How can you tell the difference between a virus and a bacterial infection on LP

A

Viral shows:
lymphocytes, normal/high protein, and HIGH glucose

Bacterial shows:
Bacteria, neutrophils, high protein and LOW glucose

Finals (32 decks)

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