Acute Care and Trauma Flashcards

1
Q

Define diabetic ketoacidosis

A

DKA is an acute metabolic complication of type 1 diabetes mellitus that is potentially fatal and requires prompt medical attention. It is characterised by absolute insulin deficiency.

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2
Q

What is the biochemical triad of diabetic ketoacidosis and describe the onset?

A

Hyperglycaemia
Ketonaemia
Acidaemia

There is RAPID onset.

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3
Q

Summarise the epidemiology of diabetic ketoacidosis?

A

In DKA, there is a reduction in the net effective concentration of circulating insulin and an elevation of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone).
This leads to metabolic derangements and ketone production.

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4
Q

What are common precipitating events of DKA and risk factors?

A

Two most common precipitating factors:
Inadequate insulin therapy
Infection

Other risk factors:
Underlying medical conditions eg MI or stroke - release of counter-regulatory hormones
Drugs that affect carbohydrate metabolism (corticosteroids, thiazides, pentamidine, sympathomimetic agents, second-generation antipsychotic agents)
SGLT-2 inhibitors
Pancreatitis
Acromegaly
Hyperthyroidism
Cushing's Syndrome
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5
Q

Summarise the epidemiology of DKA

A

Less common with increasing age

0-128 per 1000 people

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6
Q

What are the presenting symptoms of DKA?

A
Polyuria
Polyphagia
Polydipsia
Weight loss
Weakness
Nausea and vomiting
Abdominal pain
Drowsiness
Confusion
Coma
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7
Q

What are the signs on physical examination of DKA?

A

Signs of dehydration - dry mucous membranes, poor skin turgor, sunken eyes
Tachycardia
Hypotension
Kussmal respiration - rapid and deep respiration due to acidosis
Acetone breath
Hypothermia

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8
Q

What are appropriate investigations for DKA?

A
Bloods:
PLASMA GLUCOSE - high (>13.9mmol/L)
Capillary or serum KETONES - BOHB >3.8mmol/L
SERUM UREA - elevated due to volume depletion
SERUM CREATININE - elevated
Serum sodium - low
Serum potassium - elevated
FBC - elevated WCC

ABG - acidosis, low bicarbonate
URINALYSIS - positive for glucose and ketones, in presence of infection positive for leukocytes and nitrites

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9
Q

What is the management of DKA?

A

Intravenous fluids (0.9% saline)
Supportive care (ICU admission)
Potassium therapy if hypokalaemic (often caused by insulin therapy and correction of acidaemia)
IV dextrose when glucose reaches 15mmol/L

Intravenous insulin once serum potassium normalises
Add vasopressors, bicarbonate therapy and phosphate therapy

Monitor blood glucose, ketones, urine output and VBG

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10
Q

What are the possible complications of DKA?

A

Hypoglycaemia if excessive insulin therapy
Hypokalaemia due to bicarbonate and insulin therapy
Thromboembolic events - give heparin prophylaxis
Non-anion gap hypercholaraemic acidosis – due to urinary loss of ketoanions
Cerebral oedema
Acute Respiratory Distress Syndrome

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11
Q

What is the prognosis of DKA?

A

Mortality rate of 5%

Prognosis worse at age extremes or in presence of coma or hypotension

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12
Q

Define anaphylaxis

A

A severe hypersensitivity reaction characterised by rapidly developing life-threatening breathing or circulation problems and an associated urticarial skin rash.

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13
Q

Summarise the aetiology of anaphylaxis

A

Hypersensitivity of the immune system to a non-harmful antigen resulting in mast cell and basophil degranulation
Histamine causes bronchi and GI smooth muscle constriction and blood vessel dilation and permeability

Mainly IgE antibody mediated
In rare cases, immune complex mediated (opioids, contrast medium)
Can be non-immunologic

Causes:
Food allergy - shellfish, peanuts, eggs
Bee sting
Drugs - antibiotics eg penicillin, NSAIDs
Latex
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14
Q

Summarise the epidemiology of anaphylaxis

A

Food allergy anaphlyaxis most common in young children
Food allergy affects both sexes equally
Medication most common cause in adults

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15
Q

What are the presenting symptoms of anaphylaxis?

A
Angioedema - swelling of face, eyes, mouth
Utricarial rash - red, itchy, blotchy rash with central white papule
Shortness of breath
Cough
Wheeze
Abdominal cramping
Vomiting
Diarrhoea
Pruritis
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16
Q

What are the signs on physical examination of anaphylaxis?

A
Hypotension
Tachycardia
Use of accessory muscles 
Wheeze
Stridor and hoarse voice
Chest hyperinflation
Cyanosis
Pale clammy skin
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17
Q

What are the appropriate investigations for anaphylaxis?

A

Mainly a clinical diagnosis

Serum tryptase, histamine and IgE will be raised
ABG - metabolic acidosis

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18
Q

What is the management of anaphylaxis?

A

ABCDE assessment
IM ADRENALINE
Airway support and supplemental O2
IV fluids
Antihistamine
Corticosteroids to reduce chance of biphasic reaction
Allergy testing to prevent further reactions

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19
Q

What are the possible complications of anaphylaxis?

A
MI
Loss of consciousness
Respiratory arrest
Death
Recurrence
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20
Q

What is the prognosis of anaphylaxis?

A

Individuals with previous reactions puts them at increase risk of recurrence

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21
Q

Define acute kidney injury

A

An acute decrease in kidney function, leading to an increase in creatinine and a decrease in urine outflow. This results in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.

Rise in serum creatinine of > 26micromol/L within 48 hours
Rise in serum creatinine of > 1.5 times the baseline over 7 days
Urine output <0.5ml/kg/hr for > 6 hours

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22
Q

Summarise the aetiology of acute kidney injury

A

Pre-renal:
Decreased renal perfusion - dehydration, third spacing due to sepsis or acute appendicitis, renal artery stenosis, heart failure
Hypovolaemia - acute haemorrhage, severe vomiting or diarrhoea)
Cirrhosis
Nephrotic syndrome
Hypotension - shock, sepsis, anaphylaxis
Medications - NSAIDs, ACE inhibitors, ARBs
Hepatorenal syndrome (hypoalbuminaemia due to decompensated liver failure)

Intrinsic renal:
Glomerulonephritis - nephritic or nephrotic syndrome
Nephrotoxin exposure - antibiotics, methotrexate, heavy metals
Acute interstitial nephritis (autoimmune, NSAIDs)
Glomerular: glomerulonephritis, haemolytic uremic syndrome
Tubular: acute tubular necrosis (secondary to ischaemia)
Vasculitides (e.g. Wegener’s granulomatosis)
Eclampsia

Post-renal (due to obstruction):
Urinary calculi
Prostatic cancer
BPH
Abdominal tumour eg bladder
Urethral stricture
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23
Q

Summarise the epidemiology of acute kidney injury

A

Pre-renal acute kidney injury is the most common
It is most commonly seen in adults
15% of adults admitted to hospital will develop an AKI

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24
Q

What are the presenting symptoms of acute kidney injury?

A

Depends on the underlying cause ie if urinary calculi, will have renal colic
Anuria/oligouria
ABRUPT ANURIA SUGGESTS POST-RENAL OBSTRUCTION
Confusion
Nausea/vomiting
Dehydration

25
Q

What are the signs on physical examination of acute kidney injury?

A

Hypotension
Signs of dehydration: Dry mucous membranes, postural hypotension
Tachycardia
Distended bladder if due to post-renal obstruction
Fluid overload (HF, cirrhosis, nephrotic): raised JVP, pulmonary/peripheral oedema
Pallor, rash, bruising (vascular disease)

26
Q

What are the appropriate investigations for acute kidney injury?

A

Depends on cause

Bloods:
FBC - anaemia, leukocytosis, thrombocytopenia
U&amp;Es - check for hyperkalaemia
Blood culture if suspecting sepsis
Creatinine - measure eGFR - high
PSA - elevated if BPH, prostatic cancer
ABG - metabolic acidosis

Abdo USS if suspect obstruction
CXR - pulmonary oedema
AXR - renal stones

Urinalysis - urine dip and microscopy:
Blood - nephritic cause
Leucocyte esterase and nitrites - UTI
Glucose, protein and urine osmolality

Immunology:
Serum immunoglobulins and protein electrophoresis: for multiple myeloma and Bence-Jones proteins in the urine
ANA and anti-dsDNA: associated with SLE
Complement levels: low in active lupus
Anti-GBM antibodies: Goodpasture’s syndrome
Antistreptolysin-O antibodies: high after Streptococcal infection
Virology: check for hepatitis and HIV

27
Q

What is the management of acute kidney injury?

A
  1. Avoid nephrotoxic agents
    - Remove drugs such as antibiotics, NSAIDs, ACEi
    - No radiocontrast procedures
  2. Manage fluid levels
    - If signs of dehydration - IV fluids eg saline, vasopressors eg noradrenaline
    - If signs of fluid overload - fluid restriction, furosemide
  3. Protect from hyperkalaemia
    - Give IV calcium gluconate - protect heart
    - Give IV insulin and glucose
  4. Dialysis if AKI refractory to treatment
    Indications: Refractory hyperkalaemia, Refractory pulmonary oedema, metabolic acidosis, uraemic complications eg pericarditis, uraemic encephalopathy

Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrology if intrinsic renal disease is suspected

28
Q

What are the possible complications of acute kidney injury?

A
Metabolic acidosis
Hyperkalaemia
Uraemic complications - pericarditis, uraemic encephalopathy
Fluid overload
CKD
End stage renal disease
Pulmonary oedema
29
Q

What is the prognosis of acute kidney injury?

A

Inpatient mortality varies depending on cause and comorbidities
Indicators of poor prognosis: Age, multiple organ failure, oliguria, hypotension, CKD
Patients who develop AKI are at increased risk of developing CKD
Irreversible in 5-7% of adults

30
Q

Define burns

A

Burns are very common injuries, predominantly to the skin and superficial tissues, caused by heat from hot liquids, flame, or contact with heated objects, electrical current, or chemical.
Severity is assessed by burn size (% total body surface area) and depth (first to fourth degree).

31
Q

Summarise the aetiology of burns

A

Thermal burns: heat from hot liquids, flame, or contact with heated objects
Young children - 70% of burns caused by scalding from hot liquids
Older children and young working adults, flame injuries are more likely
Older adults, scalds and cooking accidents are most common

Electrical burns
Chemical burns: exposure to industrial or household chemical products

Non-accidental burns: Approximately 20% of burns in younger children involve abuse or neglect

Radiation burns

32
Q

Summarise the epidemiology of burns

A

Difficult to determine as many people do not seek medical help
250,000 people suffer burn injuries in the UK

33
Q

What are the presenting symptoms and signs on physical examination of burn injuries?

A

1st degree burns - dry, red, painful, blanching skin affected
2nd degree - red, clear blisters, wet, weepy, blanching, painful
2nd degree deep partial thickness - colour variation (white, red, yellow), blisters, may not blanch
3rd degree - dry, waxy white, leathery grey, no blanching, stiff, inelastic, pain due to deep pressure
4th degree - charred black, dry, patches of dead skin

Blistering sloughing skin
Underlying wet, tender erythema
Flame injury can present with leathery burns

34
Q

What are the appropriate investigations of burn injuries?

A
Mainly clinical diagnosis
FBC:
Low haematocrit
Hypovolaemia
Neutropenia
Thrombocytopenia 

Metabolic panel:
High urea, creatinine, glucose
Hyponatraemia
Hypokalaemia

Carboxyhaemoglobin high if inhalational injury
ABG - metabolic acidosis if inhalational injury

Wound biopsy and histology if suggestions of infection

35
Q

Define aspirin overdose

A

Excessive ingestion of aspirin causing toxicity

> 150mg/kg/day

Severity is dose-dependent
>150mg/kg: mild
>250mg/kg: moderate
>500mg/kg: severe
>700mg/kg: potentially fatal
36
Q

Summarise the aetiology of aspirin overdose

A

Accidental ingestion
Self-harm
Attempted suicide
Incorrect dosage in children or older adults

Salicylate activates respiratory centre - causes respiratory alkalosis
Compensatory urinary excretion of bicarbonate and potassium - METABOLIC ACIDOSIS

37
Q

Summarise the epidemiology of aspirin overdose

A

One of the most common drug overdoses
Accidental overdose in children and overdose for attempted suicide decreased following introduction of maximum number of aspirin you could purchase

38
Q

What are the presenting symptoms of aspirin overdose?

A
Initially asymptomatic
Fever, sweating, flushing
Nausea, vomiting, dehydration, epigastric pain
Tinnitus, deafness, vertigo
Shortness of breath
Late stages:
Lethargy
Confusion
Convulsions
Coma
Respiratory distress
Drowsiness

Rare: non-cardiogenic pulmonary oedema

39
Q

What are the signs on physical examination of aspirin overdose?

A

Tachypnoea
Tachycardia
Fever
Epigastric tenderness

40
Q

What are the appropriate investigations of aspirin overdose?

A

Serum salicylates - elevated
Serum ketones - elevated
ABG - respiratory alkalosis followed by metabolic acidosis
Electrolytes - hypokalaemia, hypocalcaemia, hypomagnesaemia
LFTs - elevated AST and ALT if hepatotoxicity
Clotting - elevated PT
Toxicology
CXR - pulmonary oedema

ECG - hypokalaemia - small T waves, U waves

41
Q

Define opiate overdose

A

Ingestion of a larger quantity of opioids that can be physically tolerated, resulting in dangerous CNS and respiratory depression, miosis and apnoea

42
Q

Summarise the aetiology of opioid overdose

A

Substance abuse in regular users of illict or prescription opioids
Unintentional overdose for pain relief
Intentional overdose - self-harm, suicide
Iatrogenic
Recent abstinence in chronic users leading to decreased tolerance

Increased toxicity at lower dose due to:
Hypothyroidism
Hypotension
Asthma
Renal or hepatic impairment
Risk Factors:
Mental health conditions
Alcoholics
Opioid abuse and dependence
Recent abstinence in chronic users
Morphine toxicity at a lower dose
43
Q

Summarise the epidemiology of opioid overdose

A

The elderly are at greater risk because they are more likely to be on opiates
Heroin and morphine are responsible for most drug-related deaths
Most common cause of death of former inmates after leaving prison due to loss of tolerance

44
Q

What are the presenting symptoms of opioid overdose?

A
Constipation (decreased GI motility if chronic)
Altered mental status
Coma
Pink frothy sputum if causes ARDS
Seizures
Nausea and vomiting 
Loss of appetite
Sedation
Craving the next dose
Drowsiness (if acute overdose)
45
Q

What are the signs on physical examination of opioid overdose?

A
Miosis/pinpoint pupils
Bradypnoea (reduced RR)
Needle or track marks
Pulmonary rales if causes ARDS
Respiratory depression 
Hypotension and tachycardia
46
Q

What are the appropriate investigations of opioid overdose?

A

Toxicology screen
Therapeutic trial with IV naloxone (opioid antagonist) - shows reversal of overdose symptoms
ECG - check for myocardial ischaemia
CXR - may show ARDS

47
Q

Define paracetamol overdose

A

Excessive ingestion of paracetamol causing toxicity

Acute overdose is ingestion >4g or >75mg/kg in <1 hour

48
Q

Summarise the aetiology of paracetamol overdose

A

Intentional overdose - self-harm or suicide
Therapeutic error - consistently taking small amounts over appropriate dosage
Incorrect dosing

The maximum recommended dose is 2 x 500 mg tablets (allows 4 times in 24 hours)
Intake > 12 g can cause hepatic necrosis

Risk Factors:
Chronic alcohol abusers
History of self-harm
History of frequent or repeated use of medications for pain relief
Patients on enzyme-inducing drugs (e.g. anticonvulsants)
Malnourished
Anorexia nervosa
Pre-existing liver disease
Acute or chronic starvation
49
Q

Summarise the epidemiology of paracetamol overdose

A

Paracetamol is the most common drug used in overdose in the UK - 48% of poisoning admissions to hospital
Causes 100 deaths per year in the UK

50
Q

What are the presenting symptoms of paracetamol overdose?

A

First 24 hours:
Asymptomatic
Mild GI disturbance - nausea, vomiting, anorexia, abdominal pain, lethargy, malaise

24-72 hours:
RUQ pain
Vomiting

72+ hours:
Increased confusion (encephalopathy)
Jaundice
Decreased consciousness level
Asterixis
51
Q

What are the signs on physical examination of paracetamol overdose?

A

Less than 24 hours: no signs

24-72 hours: hepatomegaly, RUQ tenderness

72+ hours: jaundice, coagulopathy, hypoglycaemia, renal angle tenderness, asterixis

52
Q

What are the appropriate investigations for paracetamol overdose?

A

Serum paracetamol - peak levels 4hrs after ingestion
AST and ALT - elevated
Arterial pH and lactate - acidaemia and elevated lactate
U+Es - renal impairment
PT - prolonged
INR - increased

53
Q

Define thalassaemia

A

An autosomal recessive disorder caused by defective globin chain synthesis, due to reduced or absent alpha or beta chains.

54
Q

Summarise the aetiology of thalassemia

A

Alpha:
Autosomal recessive mutation in one of the 4 alpha genes on chromosome 16
1 abnormal gene = asymptomatic silent carrier
2 abnormal genes = alpha thalassemia minor, mild microcytic anaemia
3 abnormal genes = HbH disease/alpha thalassemia major, microcytic anaemia and hepatosplenomegaly
4 abnormal genes = Hb Bart’s hydrops fetalis - incompatible with life

Beta:
Autosomal recessive mutation in one of the beta genes on chromosome 11
1 gene with reduced or absent synthesis - beta thalassemia minor
2 genes with reduced synthesis = beta thalassemia intermedia
2 genes with absent synthesis = beta thalassemia major

55
Q

Summarise the epidemiology of thalassemia

A

More common in Africa, Mediterranean and South-East Asia

56
Q

What are the presenting symptoms of thalassemia?

A

Alpha thalassemia minor and HbH disease:
Pallor
Shortness of breath
Fatigue

Beta thalassemia major:
Pallor
Shortness of breath
Fatigue
Jaundice
Ascites
Growth retardation
Symptoms of haemochromatosis
Failure to thrive
Prone to infection

Alpha and beta trait:
May be asymptomatic
Detected in routine bloods or due to family history

57
Q

What are the signs on physical examination of thalassemia?

A
Beta thalassemia major:
Ascites
Hepatosplenomegaly
Jaundice
Enlarged head and cheeks - chipmunk facies
Pallor
Frontal bossing
58
Q

What are the appropriate investigations for thalassemia?

A

FBC - microcytic anaemia, decreased MCH
Peripheral blood smear: microcytic hypochromic RBCs, target cells, golf ball-like cells in alpha thalassemia, high reticulocyte count
Hb electrophoresis:
Alpha - HbH band in HbH disease
Beta - decreased HbA, increased HbF and HbA2
Genetic testing

Beta thalassemia major:
Unconjugated bilirubin - elevated
LDH - elevated
Serum iron, ferritin and transferrin - increased
Abdo USS - hepatosplenomegaly
Skull X-Ray - hair on end sign

Bone Marrow biopsy - Hypercellular, erythroid hyperplasia