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Emergency Notes Flashcards

1
Q

What is the acronym to assess breathing?

A

RATES - Rate, auscultate, trachea, effort, SpO2.

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2
Q

What Investigations do you order for trauma patient?

A

FBC, UEC< LFT< Lipase, Coags, G+H
CXR - haemothorax
FAST - Focused Assessment with sonography in Trauma - intra-abdominal blood and cardiac tamponade
Pelvic XR - Pelvic CTA

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3
Q

What is the coagulopathy of trauma?

A

A lethal triad of:
Acidosis - causes clotting factor dysfunction. Inadequate tissue perfusion in hypovolaemic shock - metabolic acidoses. Resp issues - resp acidosis
Hypothermia - platelet dysfunction, enzymatic function disrupted. Acidosis and hypothermia are synergist and when both present worsen coagulopathy more.
Haemodilution - fluid administration. Iatrogenic coagulopathy. Alterations in the coag system induced by large volumes of IV fluids or unbalanced components of blood administration.

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4
Q

How many stages of haemorrhagic shock are there?

A

4

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5
Q

What 8 factors change through the stages of haemorrhagic shock?

A

Blood loss (mL)
%Blood loss
Pulse
BP
Pulse pressure
RR
Urine output
CNS

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6
Q

Describe the first stage of haemorrhagic shock.

A

Less than 750mL blood loss (less than 15%). Pulse less than 100, BP is normal, Pulse pressure is normal or elevated, RR is 14-20, Urine output is over 30 mL/hr, CNS is slightly anxious.

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7
Q

Describe the second stage of haemorrhagic Shock

A

Blood loss 750-1500 mL, 15-30%. Pulse 100-120, N BP, decreased pulse pressure, RR 20-30, Urine output 20-30 mL/hr, Mildly anxious.

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8
Q

Describe the third stage of Haemorrhagic shock.

A

1500-2000 mL blood loss (30-40%), 120-140 PR, lowered blood pressure, lowered pulse pressure, 30-40 RR, 5-15 ml/hr of urine output, and confused.

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9
Q

Describe the fourth stage of haemorrhagic shock.

A

Over 2L blood loss, over 40%. Over 140 HR, with lowered BP and pulse pressure. Over 35 RR, Neglible urine output and confused and lethargic CNS.

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10
Q

What is a major trauma?

A

Major injury affecting more than one body system or
Injury severity score over 15.

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11
Q

What is the trauma call criteria?

A

Mechanism: Fall over 6m, high risk MVC, MBC, vehicle vs pedestrian.
Specific injuries: Flail chest, paralysis, proximal penetrating injuries or amputations, pelvic fractures, multiple long bone fractures, crushed or mangled extremity.
Physiological derangement: GCS less than 14, SBP less than 90, RR over 30 or less than 10.
Patient factors: Extremities of age, pregnant.

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12
Q

How to fill out the injury severity score?

A

Score the worst injury at each region of the body - from No injury - minor - moderate - serious - critical - unsurvivable
Total out of 75 - Head and neck, face, chest, abdo, pelvis, extremity.

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13
Q

What are the trauma bloods?

A

FBC, UEC, VBG, Group and crossmatch, Coags, Lipase, LFTs

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14
Q

Besides trauma bloods, what other investigations would you consider for major trauma?

A

ABGs, BSL, Temp, ECG, FAST US, XR, CT, diagnostic peritoneal aspirate or diagnostic laparotomy.

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15
Q

What does TBI stand for?

A

Traumatic Brain Injury

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16
Q

How do we classify TBI?

A

Primary - injury to the brain that occurs at the time of impact or insult with immediate effects, eg direct trauma to the brain, haemorrhage, contusion, axonal shearing.
Secondary - occurs as a result of insult the the brain after the initial injury, can cause worsening damage. Eg hypotension, hypoxia, anaemia, hypercapnia, electrolyte distrubance.

Or by location:
Extradural, Subdural, subarachnoid, intraparenchymal.

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17
Q

What clinical features can you get from TBI?

A

Eyes - VI nerve palsy. Ipsilateral fixed and dilated pupils, papilledema.
Cushing’s triad
Motor and sensory abnormalities
Blood or CSF from ears
Posturing

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18
Q

What is Cushing’s Triad and what does it indicate?

A

Systolic hypertension - widening pulse pressure
Bradycardia
Respiration abnormalities - decreased or irregular

Indicates transtentorial herniation.

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19
Q

Outline the treatment for TBI

A

Head CT
ABCDE + ATLS
Secure airway, intubate, C-spine precausions
Optimise ventilation, O2, EtCO2 monitoring 30-35
IVC, maintain BP, reverse anticoagulation
BSL
Look for other injuries, normothermic

Other:
Antiemetic prophylaxis - ondansetron
Seizure Prophylaxis
Sedation if combative
Increased ICP: Head elevation to 90 degrees, Mannitol, Hypertonic saline.

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20
Q

What is Serotonin Syndrome?

A

A drug related complication resulting form increased brain stem serotonin activity, usually precipitated by the use of one or more serotonergic drugs.

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21
Q

What drugs are associated with serotonin syndrome?

A

SSRI, SNRI, MAOI, TCA
Metoclopramide, Ondansetron
Amphetamines, Opioids
St John’s Wart
CNS stimulants

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22
Q

What symptoms are associated with serotonin syndrome?

A

CNS: Headache, agitation, hypomania, confusion, hallucination, coma
Autonomic: Pupil dilation, sweating, hyperthermia, tachycardia, nausea
Somatic: Akathisia, tremor, clonus, myoclonus, hyperreflexia
Severe: Seizures, metabolic acidosis, rhabdomyolysis, Renal failure, DIC, Malignant hyperthermia.

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23
Q

What criteria are used for serotonin syndrome?

A

The Hunter Serotonin Toxicity Criteria

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24
Q

What is the antidote used in serotonin syndrome?

A

Xyproheptidine, Olanzipine, Chlorpromazine. Used for mild-moderate refractory to benzos.

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25
Q

How do you manage serotonin syndrome?

A

Cessation of serotoninergic medications
Supportive management - Benzodiazepines for clonus
Atypical antipsychotics with serotonin antagonist activity
Cyproheptadine is an antihistamine with serotonin antagonism in severe cases
Hyperthermia - benzodiazepines for muscle hyperactivity and vecuronium if severe.

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26
Q

Prognosis of serotonin syndrome?

A

Most symptoms resolve within 24 hours. But deaths have occurred.

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27
Q

What is Neuroleptic Malignant Syndrome?

A

A life threatening reaction that occurs due to Neuroleptic or antipsychotic medications.

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28
Q

What drugs can cause NMS?

A
  1. Haloperidol, droperidol, promethazine, chlorpromazine.
  2. Clozapin, olanzapine, risperidone, quetiapine
  3. Dopaminergic drugs: Levodopa on cessation, metoclopramide.
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29
Q

What is the pathophysiology of NMS?

A

Blockade of dopamine receptor D2 leading to abnormal function of the basal ganglia and muscular Sx. Atypical antipsychotics also affect serotonin, GABA and glutamate worsening the syndrome.

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30
Q

What are the symptoms of NMS?

A

FEVER - fever, encephalopathy, Vital instability (autonomic Sx), Elevated Enzymes (CK, rhabdomyolysis), Rigidity of muscles.
Can be agitated, delirious, coma, hyperkalaemia, renal failurek, seizures.
Onset within 1 week, Reaches peek in approx 3/7. Can last 8hrs - 1 month.

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31
Q

How to treat NMS?

A

Cessation of causative medication
If hyperthermic - active cooling
Symptomatic management
Dantroline for severe rigidity
?Bromocyptine

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32
Q

What is anticholinergic syndrome?

A

The inhibition of cholinergic neurotransmitters at muscarinic receptor sites following ingestion of certain medications.

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33
Q

What are the causative agents of anticholinergic syndrome?

A

Anti-histamines, anti-Parkinson’s, Atropine, Anti-spasmodics, Skeletal muscle relaxants.

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34
Q

What are the symptoms of anticholinergic syndrome?

A

Flushing, dry skin
Mydriasis
Altered Mental Status
Fever
Tachycardia and HTN
Myoclonic jerking
Urinary retention
Dysrhythmias
Seizure
“Mad as a hatter, Dry as a bone, Red as a beet, Hot as a desert, Blind as a bat”

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35
Q

What is the treatment for anticholinergic syndrome?

A

Cessation of causative agent
Supportive management
Physostigmine: Reversible acetylcholinesterase inhibitor

36
Q

Investigations for anticholinergic toxicity?

A

ECG
Temp
UEC
CK
Bladder scan
Toxicology

37
Q

What is the treatment for anticholinergic toxicity?

A

IV fluids
Activated charcoal
Whole bowel irrigation if severe
Diazepam for agitation
Avoid anticholinergic drugs
Physostigmine - reversible acetylcholinesterase inhibitor, half life 4 hours. Pts get better then deteriorate. Symptomatic management.

38
Q

What are extra-pyrimidal symptoms?

A

Drug induced movement disorders/symptoms that occur as a result of certain medications.

39
Q

What drugs cause EPS?

A

Typical and atypical antipsychotics, Metoclopramide, Antidepressants

40
Q

What symptoms are included in EPS?

A

ADAPT: Acute Dystonia, Akathisea, Parkinsonism, Tardive Dyskinesia

41
Q

What is acute dystonia?

A

Sustained or repetitive muscle contractions reslting in twisting and repetitive movements or abnormal fixed postures

42
Q

What is akathisia?

A

Feeling of inner restlessness and need to be in constant motion

43
Q

What is parkinsonism?

A

TRAP - Tremor, rigidity, akinesia (bradykinesia), postural instability.

44
Q

What is tardive dyskinesia?

A

Involuntary repetitive body movements.

45
Q

How do you monitor for EPS?

A

Abnormal Involuntary movement scale
Tool for monitoring antipsychotic effects

46
Q

What is the treatment for EPS?

A

Dose titration or cessation of causative medicine.
Anticholinergic medications
Akathisia may require B-blockers or benzos.

47
Q

What symptoms can you get if you stop antidepressants too quickly?

A

FINISH
Flu like illness
Insomnia
Nausea
Imbalance
Sensory disturbance
Hyperarousal

48
Q

What is acute cholecystitis?

A

Inflammation of the gall bladder

49
Q

What are the causes of acute cholecystitis?

A

Calculous 90% of the time.
Acalculous can be from trauma, sepsis, blood transfusion, narcotics, ABs

50
Q

What are the symptoms of acute cholecystitis?

A

Epigastric pain –> RUQ pain, worse on movement.
Billiary colic
Pain preceded by fatty foods or EtOH
Fevers, Rigors, Chills
N+V
Anorexia
Jaundice 10%
Shock
Charcot’s Triad and pentad

51
Q

What are Charcot’s Triad and pentad?

A

Tirad: RUQ Pain, Fever, leucocytosis
Pentad: Triad + Hypotension, altered consciousness.

52
Q

What clinical features to look for acute cholecystitis?

A

RQU pain worse on palpation
Garding
Murphey’s Sign
Palpable gall bladder
Febrile
Tachycardia
Peritonism

53
Q

What investigations to do for acute cholecystitis?

A

FBC
CRP
LFTs (cholestatic picure)
Increased conjugated bilirubin
US - Gall bladder wall thickening or oedema (double wall sign)
HIDA scan
CT when US unreliable (obesity)
MRI when pregnant
Cholangiogram: MRCP + ERCP + PTC (Magnetic Resonance Cholangiopancreatography + Endoscopic Retrograde cholangiopancreatography + Percutaneous transhepatic Cholangiography

54
Q

Treatment for Acute cholecystitis?

A

Supportive management: IV fluids, analgesia (buscapan), antiemetics
IVABs
Laparoscopic or open cholecystectomy. If pain settles, DC and elective. If persisten - admission and inpatient..

55
Q

What are the causes of acute pancreatitis?

A

IGETSMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Malignancy and mumps
Autoimmune
Sting - bee, scorpion, spider
Hyperlipidaemia, hypertriglyceridemia, hypercalcaemia, hyperthyroidism
ERCP
Drugs (thiazides, frusemide, azathioprine, oestrogen).

56
Q

What are the symptoms of acute pancreatisi?

A

Epigastric pain, dull and stead, progressive.
LUQ or RUQ pain
Radiation to back
N+V
Fever, chills
Shock

57
Q

What clinical features are you looking for acute pancreatitis?

A

Abdominal tenderness
Guarding
Abdominal distension
Reduced bowel sounds
Peritonitis
Hypotension and SIRS Sx
Grey-Turner’s Sign - haemorrhagic discolouration of Flanks - retroperitoneal
Cullen’s Sign - haemorrhagic discolouration of umbilicus
Hypocalcaemia

58
Q

What criteria do you use for acute pancreatitis?

A

Atlanta Criteria: 2/3
Classic abdominal pain
Lipase 3x upper limit normal
Imaging suggestive of pancreatitis

59
Q

Investigations for acute pancreatitis:

A

Bloods: FBC, CRP, Lipase, LFTs, Electrolytes, UECs, urine output.
Imagine: US, CT, MRI, ?CXR to exclude other pathology.

60
Q

How to treat acute pancreatitis?

A

Fluid Resus
Analgesia, NPO, Antiemetics
Electrolyte monitoring and replacement
ABs (Tazocin)
Surgical intervention when severe or due to gallstones

61
Q

What are the complications of acute pancreatitis?

A

Peripancreatic fluid collection, pseudocyst, pancreatic abscess
Intra-abdominal infection
Infected necrosis
Splanchnic thrombosis
Abdominal compartment syndrome
Pleural effusion
Shock

62
Q

What is appendicitis?

A

Inflammation of the veriform appendix usually due to appendiceal luminal obstruction.

63
Q

What symptoms can you get for appendicitis?

A

Epigastric pain, severe, intermittent, dull. Moves to the RLQ, sharp pain, increasing in severity, constant.
N, V, A
Fever, malaise
Constipation is late.

64
Q

What clinical features do you look for in appendicitis?

A

Peritonism, guarding, rigidity, rebound tenderness, diminished bowel sounds on the right, shock.
McBurney’s Point - Pain on palpation - worse 3.8-5cm along line ASIS to umbilicus
Rovsing’s Sign - RLQ pain with palpation of LLQ
Psoas Sign: Pt lies on left and passive attempt to extend R hip, painful is positive
Obturator sign: Internal rotation of thigh causes pain
Markle sign: Pain in abdominal cavity when dropping from toes to heels.

65
Q

What score do we use for appendicitis?

A

MANTRELS score:
Migration of pain to RLQ
Anorexia
N+V
Tenderness in RLQ (2)
Rebound tenderness
Elevated Temp
Leucocytosis (2)
Shift of WBC to left

66
Q

What investigations to do for appendicitis?

A

FBC
Inflammatory markers
UA
Pregnancy test
US
CT
Diagnostic laparoscopy

67
Q

Treatment for appendicitis?

A

Analgesia
Fluid resus
NPO
IVABs (gm-ve and anaerobic coverage)
Lap appendectomy

68
Q

What are the types of acute infectious diarrhoea?

A

Actue: 3 days to 14 days
Chronic: Over 14 days loose stools

69
Q

What are the symptoms of gastroenteritis?

A

Diarrhoea, N+V, Fever, Generally unwell, crampy abdominal pain, dehydration

70
Q

What are the causes of gastroenteritis?

A

Viral: Norovirus, Rotavirus, Adenovirus
Parasitic: Giardia lamblia, entamoeba histolitica
Bacterial: E Coli, Campylobacter Jejuni, Salmonella, Shigella, Clostridium Difficile

71
Q

What is the treatment for gastroenteritis?

A

Fluid and electrolyte replacement
Bacterial: ABs.

72
Q

Causes of small bowel obstruction?

A

HAVIT: Hernia, Adhesions, Volvulus, Intussusception, Tumour

73
Q

What is a TIA?

A

Sudden onset focal neurological Sx caused by transient decreased blod flow, lasting for less than 24 hours resolving with no permanent neurological symptoms.

74
Q

Describe the pathophysiology of a TIA.

A

TIAs are characterised by a temporary reduction or cessation of cerebral blood flow in a psecific neurovascular distribution as a result of partial or total occlusion - typically from an acute thromboembolic event or stenosis of a small penetrating vessel that resolves spontaneously with no remaining neurological deficit.

75
Q

What are the causes of TIA?

A

Atherosclerosis
Embolic source - AF, valvular disease, mural thrombus, paradoxial embolism
Arterial dissection
Hypercoagulable states
Unknown

76
Q

What are some risk factors for TIAs?

A

AF
hypercoagulability
valvular disease
carotid stenosis
CCF
HTN
DM
EtOH
Smoking
Age

77
Q

What score can be used for TIA?

A

ABCD2 score - risk stratification for CVA post TIA. 6-7 = 8% risk of CVA within 2 days.
Age over 60
BP over 140/90
Clinical features:
Unilateral weakness (2)
Speech impairment without unilateral weakness
Duration
over 60mins, (2)
10-59 mins (1)
Diabetes

78
Q

What investigations for TIA?

A

FBC, UEC, Coags, Head CT - non-con, CT angiogram, MRI, ECG - cardioembolic cause

79
Q

How to treat for TIA?

A

Treat as a stroke until proven otherwise.
Antiplatelet - aspirin 100 mg or clopidogrel 75 mg
Anticoagulant: NOACs
Mx of risk factors / causes

80
Q

What is an ischaemic stroke?

A

Sudden loss of blood circulating in an area of arterial blockage causing ischaemia, cell death and corresponding loss of neurological function. Acute neurological deficit lasts over 24 hours.

81
Q

What are the causes of ischaemic stroke?

A

Thrombus
Embolic - clot, cholesterol, fat, air, placenta, septic, malignant
Cardioembolic
Vasculitis
Hypercoagulability
Dissection
Moyamoya disease

82
Q

What are the DDx for stroke?

A

TIA, hypoglycaemia, seizure, Bell’s palsy, infection, brain neoplasm, migraine

83
Q

What is an extradural haemorrhage?

A

Bleeding between the inner surface of the skull and outer dura mata.

84
Q

What is an extradural haemorrhage associated with?

A

Commonly with trauma.
Frequently associated with a skull # of the temporal bone 75%
Tearing to the middle meningeal artery 75%
Can occur due to torn venous sinus and overlying #

85
Q

What symptoms are common with extradural haemorrhage?

A

Hx of head trauma
LOC
Lucid interval
Headache
N+V
Seizure
Decreased level of consciousness

86
Q

What clinical features are common with extradural haemorrhage?

A

skull contusion, laceration, bleeding
Decreased level of Consciousness
Cushing’s triad
Hemiplegia
Postruing
Sluggish pupils
CNIII palsy - oculomotor. Dilated ipsilateral pupil, can progress to bilateral.
CNVI Palsy - long course. Failure of lateral gaze
Fixed dilated pupil - ipsilateral or bilateral

87
Q

What investigations to do for Extradural haemorrhage?

A

Trauma bloods
Non-con Head CT

Med (6 decks)

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