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Y3 > Acute Care & Trauma > Flashcards

Acute Care & Trauma Flashcards

1
Q

What is acute kidney injury?

A

A syndrome of decreased renal function, measured by serum creatinine or urine output, occurring over hours-days

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2
Q

Summarise the epidemiology of acute kidney injury

A

Common - occurs in up to 18% of hospital patients

50% of ICU patients

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3
Q

What are the risk factors for AKI?

A 
Hospital stay
Pre-existing CKD
Increasing age
Male
Comorbidity - CVD, malignancy, chronic liver disease, complex surgery
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4
Q

What are the commonest causes of AKI?

A 
Sepsis
Major surgery
Cardiogenic shock
Other hypovolaemia
Drugs - NSAIDs, ACEis, diuretics
Hepatorenal syndrome
Obstruction
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5
Q

How can the causes of AKI be categorised?

A

Pre-renal: decreased kidney perfusion
Renal: intrinsic renal disease
Post-renal: obstruction to urine

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6
Q

What are the presenting signs + symptoms of AKI?

A 
May be asymptomatic at first
Decreased urine output
N + V
Dehydration
Confusion
Hypertension
Abdo + back pain
Oedema
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7
Q

How is AKI investigated?

A

URINE DIPSTICK: proteinuria/haematuria –> intrinsic renal disease

USS: small kidneys –> CKD; asymmetry –> renal vascular disease

LFTs: check renal function - hepatorenal

Platelets: if low, need blood film to check for haemolysis (HUS/TTP)

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8
Q

How is AKI diagnosed?

A
  • Rise in creatinine > 26umol/L within 48h
  • Rise in creatinine > 1/5 x baseline (ie before AKI) within 7 days
  • Urine output <0.5mL/kg/h for >6 consecutive hours
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9
Q

How is AKI managed?

A

Pre-renal: correct volume depletion and/or increase renal perfusion via circulatory/cardiac support, treat any underlying sepsis

Renal: refer for likely biopsy and specialist treatment of intrinsic renal disease

Post-renal: catheter, nephrostomy, or urological intervention

ALL: manage fluid balance, acidosis, hyperkalaemia, and timely recognition of those who may require renal replacement (dialysis)

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10
Q

What are the complications of AKI?

A
  1. Hyperkalaemia - IV CaCl, insulin, salbutamol
  2. Pulmonary oedema - O2, diamorphine, furosemide, GTN, isosorbide dinitrate
  3. Metabolic acidosis
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11
Q

What is ARDS?

A

A non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness

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12
Q

What are the criteria for a diagnosis of ARDS?

A

Need all 3:

  1. Acute onset (within 1 week)
  2. Bilateral opacities on chest x-ray
  3. PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O
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13
Q

What are the causes of ARDS?

A

Most common cause = sepsis (septic shock), usually w pulmonary origin (e.g., pneumonia)

Pulmonary: pneumonia, gastric aspiration, inhalation, injury, vasculitis, contusion

Also: acute pancreatitis, trauma, burns, fat embolism, DIC, drugs/toxins - aspirin, heroin, paraquat, acute liver failure

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14
Q

What are the risk factors for ARDS?

A 
Sepsis
Aspiration
Pneumonia
Severe trauma
Blood transfusions
Lung transplant
Pancreatitis
EtOH misuse
Burns + smoke inhalation
Drowning
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15
Q

Summarise the epidemiology of ARDS

A

Incidence = 64/100,000
10-15% ITU patients
Increasing incidence among mechanically ventilated patients

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16
Q

What are the presenting signs of ARDS?

A 
Cyanosis
Tachypnoea
Tachycardia
Peripheral vasodilation
Bilateral fine inspiratory crackles
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17
Q

How is ARDS investigated?

A

CXR: bilateral infiltrates consistent w pulmonary oedema and not fully explained by atelectasis or pulmonary effusions

ABG: PaO2/FiO2 < 300 on PEEP/CPAP > 5cm H20 - low partial oxygen pressure

Sputum/blood/urine culture: +ve if underlying infection (sepsis)

Amylase and lipase: 3x upper limit –> acute pancreatitis

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18
Q

What is alcohol withdrawal?

A

Occurs in patients with alcohol dependence when their daily alcohol consumption is decreased or stopped

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19
Q

What causes alcohol withdrawal?

A

Abstinence from alcohol in a person with alcohol dependence

Chronic alcohol use results in upregulation of post-synaptic NMDA Rs and down-regulation of post-synaptic GABA Rs

The decrease in blood [ethanol] due to abrupt cessation in alcohol consumption –> imbalance between stimulatory (NMDA) and inhibitory (GABA) systems in CNS

Excessive stimulatory effect –> clinical signs and symptoms

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20
Q

How is alcohol withdrawal investigated?

A
  1. Serum urea + creatinine: elevated or nomal - dehydration leads to renal impairment
  2. LFTs - high or normal
  3. Toxicology screen - +ve for ethanol
  4. Electrolyte panel - metabolic acidosis, hypokalaemia
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21
Q

Summarise the epidemiology of alcohol withdrawal

A

50% of alcohol-dependent patients experience symptoms of AWS upon reduced alcohol intake

8% of hospital patients at risk of AWS

16-31% of ITU patients at risk

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22
Q

What are the presenting symptoms of alcohol withdrawal?

A

Tremor
N+V

Seizures
Hallucinations
Delusions
Fast heartbeat
Hyperthermia
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23
Q

What are the presenting signs of alcohol withdrawal?

A

Tremor
Hypertension
Memory disturbance - disoriented
Waxing + waning in level of consciousness

Seizures
Hallucinations
Delusions
Tachycardia
Hyperthermia
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24
Q

How is alcohol withdrawal managed?

A
  1. BZD - chlordiazepoxide
  2. Supportive care
  3. Phenobarbital - sedative
  4. Pabrinex
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25
Q

What are the possible complications of alcohol withdrawal?

A
  1. Over-sedation
  2. DT
  3. Alcohol withdrawal seizures
  4. Status epilepticus
  5. Mortality
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26
Q

What is the prognosis for alcohol withdrawal?

A

Persistent insomnia + autonomic symptoms for a few months after acute withdrawal phase

Usually last for 6 months

50% patients remain abstinent for a year

Relapse prevention w counselling, self-help groups, pharmacotherapy

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27
Q

What are the risk factors for alcohol withdrawal syndrome?

A

Hx of AWS and DT

Abrupt withdrawal of alcohol

28
Q

What is anaphylaxis?

A

An acute, severe, life-threatening allergic reaction in pre-sensitised individuals, leading to a systemic response caused by the release of immune and inflammatory mediators from basophils and mast cells.

At least 2 organ systems involved

29
Q

What are the causes of anaphylaxis?

A

Exposure to allergen in pre-sensitised individuals

Common allergens = drugs, foods, insect stings, exercise

30
Q

What are the risk factors for anaphylaxis?

A

<30 yo: food-associated, exercise-induced

Atopy/asthma

Hx of anaphylaxis

Exposure to common sensitiser

31
Q

Summarise the epidemiology of anaphylaxis

A

Under-reported

Prevalence = 1-17%

Adults - drug- and vaccine-induced reactions - pencillin, NSAIDs

Kids - food

32
Q

What are the presenting symptoms of anaphylaxis?

A 
Itching
Sweating
Diarrhoea
Vomiting
Difficulty breathing
33
Q

What are the presenting signs of anaphylaxis?

A 
Hyperhidrosis
Erythema
Urticaria
Oedema
Wheeze
Laryngeal obstruction
Cyanosis
Tachycardia
Hypotension
34
Q

How is anaphylaxis investigated?

A

Serum tryptase: elevated

In vitro IgE: >0.35 = atopy
Skin test: >3mm diameter
Challenge test: objective symptoms of allergy response

35
Q

How is anaphylaxis managed?

A
  1. Cardiorespiratory assessment + supportive measures
  2. IM adrenaline
  3. Assess + secure airway
  4. IV normal saline

If hypotensive + glucagon
If persistent resp symps + inhaled SABA - salbutamol
Hives + rhinorrhoea - H1+2 antagonist (diphenhydramine)
Post-emergency stabilisation: Prednisolone

Ongoing: immunotherapy

36
Q

What are the possible complications of anaphylaxis?

A
  1. MI
  2. Death - following CV shock or cardiac arrest if delay in IM adrenaline administration
  3. Recurrence
37
Q

What is the prognosis for anaphylaxis?

A

Individuals w previous reactions are at higher risk of recurrence

Outlook depends on success of immune therapy, allergen avoidance, and compliance with carrying epipen

38
Q

What is ABG?

A

An arterial blood glass test measures the pH and levels of oxygen and carbon dioxide in the blood from an artery

39
Q

What is an ABG used for?

A

To check how well the lungs are able to move oxygen into and remove carbon dioxide from the blood

40
Q

What are the indications for an ABG?

A
  • Any unexpected deterioration in ill patient
  • Acute exacerbation of chronic chest condition
  • Impaired consciousness or respiratory effort
  • Signs of CO2 retention
  • Cyanosis, confusion, visual hallucinations (signs of low PaO2)
  • To validate measurements from transcutaneous pulse oximetry
41
Q

What are the signs of CO2 retention?

A

Bounding pulse
Drowsy
Tremor (flapping)
Headache

42
Q

What are the possible complications of an ABG?

A 
Local haematoma
Arterial vasosapsm
Arterial occlusion
Air or thrombus embolism
Local anaesthetic anaphylactic reaction
Infection
Needle stick injury
43
Q

What is aspirin overdose?

A

Salicylate poisoning

The result of ingestion of, or topical exposure to, chemicals metabolised to salicylate

44
Q

What are the risk factors for aspirin overdose?

A
  • Ingestion of 150mg/kg or more, or 6.5g or more, of aspirin or aspirin-equivalent
  • Children < 3yo
  • Adults < 70yo
  • Hx of self-harm or suicide attempt
45
Q

What causes aspirin overdose?

A

Acetylsalicylic acid (aspirin) is rapidly hydrolysed to salicylate in the GIT and bloodstream

46
Q

What are the signs of aspirin overdose?

A 
Unexplained delirium
Fever
Diaphoresis
Tachypnoea
Hyperpnoea
Kussmaul's breathing
Movement disorders, asterixis, stupor
Confusion and/or delirium
Coma and/or papilloedema
Volume depletion
47
Q

How is aspirin overdose investigated?

A
  1. ABG
  2. Serum electrolyte panel
  3. Serum salicylate level
  4. Serum urea + creatinine
48
Q

What are the possible acute complications of a blood product transfusion?

A

Acute haemolytic reaction
Allergic reaction
Anaphylactic reaction
Coagulation problems in massive transfusion
Febrile non-haemolytic reaction
Metabolic derangements
Mistransfusion (incorrect product)
Septic/bacterial contamination
Transfusion-associated circulatory overload
Transfusion-related acute lung injury (TRALI)
Urticarial reaction

49
Q

What are the indications for a cryoprecipitate transfusion?

A

Is high in factor VIII and fibrinogen tf used in hypofibrinogenaemia

  1. Haemorrhage after cardiac surgery
  2. Massive haemorrhage or transfusion
  3. Surgical bleeding
50
Q

What are the indications for a platelet transfusion?

A

Haemorrhage prophylaxis in patients with thrombocytopaenia or platelet function defects

51
Q

What are the possible delayed complications of a blood product transfusion?

A 
Delayed haemolytic reaction
Iron overload
Microchimerism
Overtransfusion/undertransfusion
Post-transfusion purpura
Transfusion-associated graft-versus-host disease
Transfusion-related immunomodulation
52
Q

What are the possible infectious complications of a blood product transfusion?

A 
Hep B
Hep C
Human T-lymphotrophic virus 1 or 2
HIV
Creutzfeldt-Jakob disease
Human herpesvirus 8
Malaria + babesiosis
Pandemic influenza
West Nile virus
53
Q

What is fresh frozen plasma?

A

A blood product made from the liquid portion of whole blood

54
Q

What is cryoprecipitate?

A

Frozen blood product prepared from blood plasma

High in factor 8 + fibrinogen

FFP thawed at 1-6oC
Centrifuged
Precipitate collected
Precipitate resuspended in small amount of residual plasma and then re-frozen for storage

55
Q

What is prothrombin complex concentrate?

A

AKA factor IX complex

= factors 2, (7,) 9, 10

56
Q

What are the indications for prothrombin complex concentrate?

A
  1. Prevents bleeding in haemophilia B if pure factor 9 unavailable
  2. Reverses warfarin (+ other vitamin K antagonists)
  3. Factor 2/7/9/10 deficiency
57
Q

What is burns injury?

A

Injury to the skin and superficial tissues, caused by heat from hot liquids, flames, or contact with heated objects, electrical current or chemicals

58
Q

What are the risk factors for burns injury?

A
  • Young childrne
  • Age > 60
  • Male sex
59
Q

Summarise the epidemiology of burns injury

A
  • Common
  • Death rates have been decreasing in developed countries
  • Rate of child deaths from burns is over 7x higher in developing than in developed countries
  • 250,000 per year in UK
  • Approx 175,000 to A and E
  • 13,000 admitted to hospital
60
Q

What are the causes of a burns injury?

A
  1. Thermal burns - heat, hot liquids, flame, contact w heated objects
  2. Electrical burns - caused by low-, intermediate-, and high voltage exposures
  3. Chemical burns - exposure to industrial or household chemical products
  4. Non-accidental burns - abuse or neglect in children
61
Q

How are burns classified?

A 
Superficial (1st) - epidermis
Superficial partial thickness (2nd) - extends into superficial (papillary) dermis
Deep partial thickness (2nd) - extends into deep (reticular) dermis
Full thickness (3rd) - extends through entire dermis
4th degree - extends through entire skin and into underlying fat, muscle and bone
62
Q

How is a burns injury investigated?

A

FBC - low haematocrit, hypovolaemia, neutropneia + thrombocytopenia (last 2 -sepsis)

Metabolic panel - high urea, cr, glu, hypoNa, hypoK

Carboxyhaemoglobin - high (-inhalation injury)

ABG - metabolic acidosis (-inhalation injury)

Fluorescein staining - damaged corneal epithelial cells in corneal burns

CT head spine - brain injury/fracture in cases of head or spine trauma

Wound biopsy culture/histology - sepsis?

63
Q

What are the features of a superficial burn?

A

Epidermis
Red wo blisters
Dry
Painful

64
Q

What are the features of a superficial partial thickness burn?

A 
Epidermis + superficial (papillary dermis)
Redness w clear blister
Blanches w pressure
Moist
Very painful
65
Q

What are the features of a deep partial thickness burn?

A 
Epidermis + deep (reticular) dermis
Yellow or white
Less blanching than superficial partial thickness
May blister
Fairly dry
Pressure and discomfort
66
Q

What are the features of a full thickness burn?

A 
Epidermis + entire dermis
Stiff and white/brown
No blanching
Leathery
Painless
67
Q

What are the features of a 4th degree burn?

A 
Entire skin and into underlying fat, muscle and bone
Black
Charred with eschar
Dry
Painless

Y3 (20 decks)

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