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
What are the signs on physical examination of acute kidney injury?
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
What are the appropriate investigations for acute kidney injury?
Depends on cause ``` Bloods: FBC - anaemia, leukocytosis, thrombocytopenia U&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
What is the management of acute kidney injury?
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
What are the possible complications of acute kidney injury?
``` Metabolic acidosis Hyperkalaemia Uraemic complications - pericarditis, uraemic encephalopathy Fluid overload CKD End stage renal disease Pulmonary oedema ```
29
What is the prognosis of acute kidney injury?
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
Define burns
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
Summarise the aetiology of burns
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
Summarise the epidemiology of burns
Difficult to determine as many people do not seek medical help 250,000 people suffer burn injuries in the UK
33
What are the presenting symptoms and signs on physical examination of burn injuries?
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
What are the appropriate investigations of burn injuries?
``` 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
Define aspirin overdose
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
Summarise the aetiology of aspirin overdose
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
Summarise the epidemiology of aspirin overdose
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
What are the presenting symptoms of aspirin overdose?
``` 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
What are the signs on physical examination of aspirin overdose?
Tachypnoea Tachycardia Fever Epigastric tenderness
40
What are the appropriate investigations of aspirin overdose?
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
Define opiate overdose
Ingestion of a larger quantity of opioids that can be physically tolerated, resulting in dangerous CNS and respiratory depression, miosis and apnoea
42
Summarise the aetiology of opioid overdose
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
Summarise the epidemiology of opioid overdose
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
What are the presenting symptoms of opioid overdose?
``` 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
What are the signs on physical examination of opioid overdose?
``` Miosis/pinpoint pupils Bradypnoea (reduced RR) Needle or track marks Pulmonary rales if causes ARDS Respiratory depression Hypotension and tachycardia ```
46
What are the appropriate investigations of opioid overdose?
Toxicology screen Therapeutic trial with IV naloxone (opioid antagonist) - shows reversal of overdose symptoms ECG - check for myocardial ischaemia CXR - may show ARDS
47
Define paracetamol overdose
Excessive ingestion of paracetamol causing toxicity | Acute overdose is ingestion >4g or >75mg/kg in <1 hour
48
Summarise the aetiology of paracetamol overdose
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
Summarise the epidemiology of paracetamol overdose
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
What are the presenting symptoms of paracetamol overdose?
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
What are the signs on physical examination of paracetamol overdose?
Less than 24 hours: no signs 24-72 hours: hepatomegaly, RUQ tenderness 72+ hours: jaundice, coagulopathy, hypoglycaemia, renal angle tenderness, asterixis
52
What are the appropriate investigations for paracetamol overdose?
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
Define thalassaemia
An autosomal recessive disorder caused by defective globin chain synthesis, due to reduced or absent alpha or beta chains.
54
Summarise the aetiology of thalassemia
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
Summarise the epidemiology of thalassemia
More common in Africa, Mediterranean and South-East Asia
56
What are the presenting symptoms of thalassemia?
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
What are the signs on physical examination of thalassemia?
``` Beta thalassemia major: Ascites Hepatosplenomegaly Jaundice Enlarged head and cheeks - chipmunk facies Pallor Frontal bossing ```
58
What are the appropriate investigations for thalassemia?
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