Acute Care & Trauma Flashcards
Define acute kidney injury (AKI)
An abrupt loss of kidney function resulting in the retention of urea and nitrogenous waste products and the dysregulation of extracellular volume and electrolytes. KDIGO Classification of AKI: Increase in serum creati• An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
o NOTE: this can occur in patients with previously normal kidneys or in patients with pre-existing renal disease
• KDIGO Classification of AKI
o Increase in serum creatinine > 26 mol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for 6 hours nine >26 umol/l within 48 hours/ to >1.5 times baseline within the preceeding 7 days/ urine volume <0.5 ml/kg/hr for 6 hours
Explain the aetiology / risk factors of acute kidney injury (AKI)
Pre renal (90%) - Hypovolaemia (e.g. haemorrhage, severe vomiting), heart failure, cirrhosis, nephrotic syndrome, hypotension (e.g. shock, sepsis, anaphylaxis), renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis). Intrinsic renal - glomerular - glomerulonephritis, haemolytic yuraemic syndrome, Tubular - acute interstitial necrosis, Interstitial (e.g. NSAIDs, autoimmune), Vasculitides (e.g. Wegener’s granulomatosis), Eclampsia. Post renal (due to obstruction) - Calculi, Urethral Structure, Prostatic hypertrophy or malignancy, Bladder tumour. Risk Factors: Age, CKD, Comorbidities (e.g HF), Sepsis, Hypovolaemia, Use of nephrotoxis medications, Emergency surgery, Diabetic mellitus
Summarise the epidemiology of acute kidney injury (AKI)
15% of adults admitted to hospital. Most common in the elderly.
Recognise the presenting symptoms of acute kidney injury (AKI)
Dependent on the underlying cause. Oligura/anuria (abrupt anuria suggests post-renal obstruction. Nausea/vomiting, dehydration, confusion
Recognise the signs of acute kidney injury (AKI) on physical examination
Hypertension, distended bladder, dehydration - postural hypotension, fluid overload (in HF, cirrhosis, nephrotic syndrome), - raised JVP, pulmonary and peripheral oedema, pallor, rash, bruising (vascular disease)
Identify appropriate investigations for acute kidney injury (AKI) and interpret the results
Urinalysis - blood (suggests nephritic cause), Leucocyte esterase and nitrites - UTI, Glucose, Protein, Urine osmolality. Bloods - FBC, Blood Film, U & Es, Clotting, CRP, Immunology - • Serum immunoglobulins and protein electrophoresis - for multiple myeloma - Also check for Bence-Jones proteins in the urine
• ANA - associated with SLE - Also check anti-dsDNA antibodies (high in active lupus)
• Complement levels - low in active lupus
• Anti-GBM antibodies - Goodpasture’s syndrome
• Antistreptolysin-O antibodies - high after Streptococcal infection . Virology- Hep & HIV, Ultrasound - Post renal cause - look for hydronephrosis, CXR - Pulmonary Oedema, AXR - Renal stones
Generate a management plan for acute kidney injury (AKI)
Treat the cause
FOUR main components to management:
o Protect patient from hyperkalaemia (calcium gluconate)
o Optimise fluid balance
o Stop nephrotoxic drugs
o Consider for dialysis
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
Renal Replacement Therapy (RRT) considered if:
o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications
Identify the possible complications of acute kidney injury (AKI) and its management
- Pulmonary oedema
- Acidaemia
- Uraemia
- Hyperkalaemia
- Bleeding
Summarise the prognosis for patients with acute kidney injury (AKI)
Inpatient mortality varies depending on cause and comorbidities Indicators of poor prognosis: o Age o Multiple organ failure o Oliguria o Hypotension o CKD Patients who develop AKI are at increased risk of developing CKD
Define acute respiratory distress syndrome
• A syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterised by:
o Acute onset
o Bilateral infiltrates consistent with pulmonary oedema
o Hypoxaemia
o No clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure)
o ARDS is the severe end of the spectrum of acute lung injury
Explain the aetiology / risk factors of acute respiratory distress syndrome
Severe insults to the lungs and other organs leads to the release of inflammatory mediators. These lead to increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance . Causes o Sepsis o Aspiration o Pneumonia o Pancreatitis o Trauma/burns o Transfusion o Transplantation (bone marrow and lung) o Drug overdose/reaction There are THREE pathological stages of ARDS: o Exudative o Proliferative o Fibrotic
Summarise the epidemiology of acute respiratory distress syndrome
1 in 6000
Recognise the presenting symptoms of acute respiratory distress syndrome
- Rapid deterioration of respiratory function
- Dyspnoea
- Respiratory distress
- Cough
- Symptoms of CAUSE
Recognise the signs of acute respiratory distress syndrome on physical examination
- Cyanosis
- Tachypnoea
- Tachycardia
- Widespread inspiratory crepitations
- Hypoxia refractory to oxygen treatment
- Signs are usually bilateral but may be asymmetrical in early stages
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results
• CXR - bilateral alveolar infiltrates and interstitial shadowing
• Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture)
o NOTE: plasma BNP < 100 pg/mL could distinguish ARDS from heart failure
• Echocardiography
o Check for severe aortic or mitral valve dysfunction
o Low left ventricular ejection fractions = haemodynamic oedema rather than ARDS
• Pulmonary Artery Catheterisation
o Check pulmonary capillary wedge pressure (PCWP)
• Bronchoscopy
o If the cause cannot be determined from the history
Define adrenal insufficiency
Deficiency of adrenal cortical hormones (e.g. mineralocorticoids, glucocorticoids and androgens)
Explain the aetiology / risk factors of adrenal insufficiency
Primary Adrenal Insufficiency o Addison's disease (usually autoimmune) Secondary Adrenal Insufficiency o Pituitary or hypothalamic disease Infections o Tuberculosis o Meningococcal septicaemia (Waterhouse-Friderichsen Syndrome) o CMV o Histoplasmosis Infiltration o Metastasis (mainly from lung, breast, melanoma) o Lymphomas o Amyloidosis Infarction o Secondary to thrombophilia Inherited o Adrenoleukodystrophy o ACTH receptor mutation Surgical o After bilateral adrenalectomy Iatrogenic o Sudden cessation of long-term steroid therapy
Summarise the epidemiology of adrenal insufficiency
- Most common cause is IATROGENIC
* Primary causes are rare
Recognise the presenting symptoms of adrenal insufficiency
• Chronic Presentation - the symptoms tend to be VAGUE and NON-SPECIFIC o Dizziness o Anorexia o Weight loss o Diarrhoea and Vomiting o Abdominal pain o Lethargy o Weakness o Depression • Acute Presentation (Addisonian Crisis) o Acute adrenal insufficiency o Major haemodynamic collapse o Precipitated by stress (e.g. infection, surgery)
Recognise the signs of adrenal insufficiency on physical examination
• Postural hypotension • Increased pigmentation o More noticeable on buccal mucosa, scars, skin creases, nails and pressure points • Loss of body hair in women (due to androgen deficiency) • Associated autoimmune condition (e.g. vitiligo) • Addisonian Crisis Signs o Hypotensive shock o Tachycardia o Pale o Cold o Clammy o Oliguria
Identify appropriate investigations for adrenal insufficiency and interpret the results
To confirm the diagnosis
9 am Serum Cortisol (< 100 nmol/L is diagnostic of adrenal insufficiency)
• > 550 nmol/L makes adrenal insufficiency unlikely
Short Synacthen Test
• IM 250 g tetrocosactrin (synthetic ACTH)
• Serum cortisol < 550 nmol/L at 30 mins indicates adrenal failure
Identify the level of the defect in the hypothalamo-pituitary-adrenal axis
o HIGH in primary disease
o LOW in secondary
Long Synacthen Test
• 1 mg synthetic ACTH administered
• Measure serum cortisol at 0, 30, 60, 90 and 120 minutes
• Then measure again at 4, 6, 8, 12 and 24 hours
• Patients with primary adrenal insufficiency show no increased after 6 hours
Identify the cause
o Autoantibodies (against 21-hydroxylase)
o Abdominal CT or MRI
o Other tests (adrenal biopsy, culture, PCR)
Check TFTs
Investigations in Addisonian crisis
o FBC (neutrophilia –> infection)
o U&Es
• High urea
• Low sodium
• High potassium
o CRP/ESR
o Calcium (may be raised)
o Glucose - low
o Blood cultures
o Urinalysis
o Culture and sensitivity
Generate a management plan for adrenal insufficiency
Addisonian Crisis
o Rapid IV fluid rehydration
o 50 mL of 50% dextrose to correct hypoglycaemia
o IV 200 mg hydrocortisone bolus
o Followed by 100 mg 6 hourly hydrocortisone until BP is stable
o Treat precipitating cause (e.g. antibiotics for infection)
o Monitor
Chronic Adrenal Insufficiency
o Replacement of:
• Glucocorticoids with hydrocortisone (3/day)
• Mineralocorticoids with fludrocortisone
o Hydrocortisone dosage needs to be increased during times of acute illness or stress
o NOTE: if the patient also has hypothyroidism, give hydrocortisone BEFORE thyroxine (to prevent precipitating an Addisonian crisis)
Advice
o Have a steroid warning card
o Wear a medic-alert bracelet
o Emergency hydrocortisone on hand
Identify the possible complications of adrenal insufficiency and its management
HYPERKALAEMIA
Death during Addisonian crisis
Summarise the prognosis for patients with adrenal insufficiency
• Adrenal function rarely recovers • Normal life expectancy if treated Autoimmune Polyendocrine Syndrome Type 1 - autosomal recessive disorder caused by mutations in the AIRE gene. Consists of the following diseases: • Addison's disease • Chronic mucocutaneous candidiasis • Hypoparathyroidism Type 2 - also known as Schmidt's Syndrome • Addison's disease • Type 1 Diabetes • Hypothyroidism • Hypogonadism
Define alcohol withdrawal
The symptoms that may occur when a person has been drinking too much alcohol on a regular basis and suddenly stops drinking.
Explain the aetiology / risk factors of alcohol withdrawal
Chronic alcohol consumption suppresses the activity of glutamate (an excitatory neurotransmitter), so the body compensates by increasing sensitivity to glutamate
So, when alcohol consumption stops, you get increased glutamate activity leading to excitatory symptoms
Summarise the epidemiology of alcohol withdrawal
If untreated, 6% of alcohol-dependent patients develop clinically relevant symptoms of withdrawal
Up to 10% of them will delirium tremens
Recognise the presenting symptoms of alcohol withdrawal
History of high alcohol intake Mild Symptoms: o Insomnia and fatigue o Tremor o Mild anxiety/feeling nervous o Mild restlessness/agitation o Nausea and vomiting o Headache o Sweating o Palpitations o Anorexia o Depression o Craving alcohol More severe symptoms: o Hallucinations o Withdrawal seizures (generalised tonic-clonic) Delirium tremens DEFINITION: an acute confusional sate often seen as withdrawal syndrome in chronic alcoholics and caused by sudden cessation of drinking alcohol. It can be precipitated by a head injury or an acute infection causing abstinence from alcohol.
Recognise the signs of alcohol withdrawal
FEATURES: Anxiety Tremor Sweating Vivid and terrifying visual and sensory HALLUCINATIONS (usually of animals and insects) Can be FATAL
Identify appropriate investigations for alcohol withdrawal and interpret the results
NO investigations
Generate a management plan for alcohol withdrawal
Chlordiazepoxide - reduces symptoms of alcohol withdrawal
Barbiturates may be used if refractory to benzodiazepines
Thiamine (Pabrinex) - prevents progression to Wernicke-Korsakoff syndrome
Identify the possible complications of alcohol withdrawal and its management
Patients can have seizures and die if it is left untreated
Summarise the prognosis for patients with alcohol withdrawal
Delirium tremens has a mortality of 35% if untreated
Mortality is < 2% with early detection and treatment
Define anaphylaxis
Acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation
Explain the aetiology / risk factors of anaphylaxis
Immunogenic - IgE-mediated or immune complex/complement-mediated
Non-Immunogenic - mast cell or basophil degranulation WITHOUT the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Pathophysiology
o Inflammatory mediators such as histamine are released leading to bronchospasm, increased capillary permeability and reduce vascular tone
o This leads to tissue oedema
Common Allergens
o Drugs (e.g. penicillin)
o Latex
o Peanuts
o Shellfish
o NOTE: anaphylaxis can be caused by the repeat administration of blood products in a patient with selective IgA deficiency (due to the formation of anti-IgA antibodies)
Summarise the epidemiology of anaphylaxis
COMMON
Recognise the presenting symptoms of anaphylaxis
Wheeze
Shortness of breath and a sense of choking
Swelling of lips and face
Pruritus
Rash
NOTE: patients may have a history of other hypersensitivity reactions (e.g. asthma, allergic rhinitis)
Recognise the signs of anaphylaxis on physical examination
Tachypnoea Wheeze Cyanosis Swollen upper airways and eyes Rhinitis Conjunctival infection Urticarial rash Hypotension Tachycardia
Identify appropriate investigations for anaphylaxis and interpret the results
CLINICAL diagnosis
• Serum tryptase, histamine levels or urinary metabolites of histamine may help support the clinical diagnosis
Following an attack
o Allergen skin testing - identifies allergen
o IgE immunoassays - identifies food-specific IgE in the serum
Generate a management plan for anaphylaxis
ABCDE High flow oxygen IM Adrenaline Chlorpheniramine (antihistamine) Hydrocortisone If continued respiratory deterioration, may require bronchodilator therapy Monitor pulse oximetry, ECG and BP
Identify the possible complications of anaphylaxis and its management
SHOCK
Organ damage can result from shock
Summarise the prognosis for patients with anaphylaxis
Good with prompt treatment
Define arterial blood gas
AnABGis abloodtest that measures the acidity, or pH, and the levels of oxygen (O2) and carbon dioxide (CO2) from anartery. The test is used to check the function of the patient’s lungs and how well they are able to move oxygen and remove carbon dioxide.
Summarise the indications for an arterial blood gas
Identification of respiratory, metabolic, and mixed acid-base disorders, with or without physiologic compensation, by means of pH ([H +]) and CO 2 levels (partial pressure of CO 2)
Identify the possible complications of an arterial blood gas
Patients with poor distal perfusion (eg, those in hypovolemic states, with advanced heart failure, or on vasopressor therapy) may not exhibit a strong arterial pulsation; the operator may need to pull back the ABG syringe plunger to get a blood sample, though this increases the risk of venous blood sampling
If arterial blood flow is not obtained, the operator might slowly pull back the needle; it is possible that the needle has gone through the vessel
Initial arterial flow may subsequently be lost if the needle moves outside the vessel lumen; reidentification of the arterial pulse, using the nondominant middle and index finger, and repositioning the needle in the direction of the vessel could be attempted; avoid blind movement of the needle while it is inserted deeply in the patient’s body—pull it back to a point just below the skin, and redirect it to the arterial pulse felt with the other hand
Puncture of venous structures can be identified by lack of pulsatile flow or dark-colored blood, though, arterial blood in severely hypoxemic patients can also have a dark appearance; if venous blood is obtained, removal of the needle from the patient might be necessary to expel the venous blood from the syringe
Excessive skin and abundant soft tissue may obstruct the puncture site; the operator can use the nondominant hand to smooth the skin, or an assistant can remove the subcutaneous tissue from the puncture site field
Incomplete dismissal of heparin solution from the syringe could cause falsely low values for the partial pressure of CO 2; to avoid this, the operator should expel all heparin solution from the syringe before arterial puncture
Incomplete removal of air bubbles can cause falsely elevated values for the partial pressure of oxygen; to avoid this, the operator should be sure to completely remove air bubbles from the syringe (vented plungers have an advantage over standard syringes in this regard)
Avoid puncture of the brachial artery or femoral artery in patients with diminished or absent distal pulses; the absence of distal pulses may signal severe peripheral vascular disease
When femoral or brachial artery puncture is being considered, the use of ultrasonographic guidance during passage of the needle aids in providing an accurate roadmap to the vessel and helps minimize inadvertent arterial injuries
Define aspirin overdose
Excessive ingestion of aspirin causing toxicity
Explain the aetiology / risk factors of aspirin overdose
• It can be a result of deliberate self-harm, suicidal intent or by accident
• 10-20 g can cause moderate-severe toxicity in adults
• Pathophysiology of Aspirin Overdose
Increases respiratory rate and depth by stimulating the respiratory centre
This hyperventilation –> respiratory alkalosis (in the early stage)
The body compensates by increasing urinary bicarbonate and K+ excretion
This leads to dehydration and hypokalaemia
Loss of bicarbonate, uncoupling of mitochondrial oxidative phosphorylation and the build up of lactic acid can lead to metabolic acidosis
In SEVERE cases, CNS depression and respiratory failure can occur
Summarise the epidemiology of aspirin overdose
One of the MOST COMMON drug overdoses
Recognise the presenting symptoms of aspirin overdose
Figure out the key facts: o How much aspirin was taken? o When was it taken? o Were any other drugs taken? o Have you had any alcohol? The patient may initially be asymptomatic Early Symptoms o Flushed o Fever o Sweating o Hyperventilation o Dizziness o Tinnitus o Deafness Later Symptoms o Lethargy o Confusion o Convulsions o Drowsiness o Respiratory depression o Coma
Recognise the signs of aspirin overdose on physical examination
- Fever
- Tachycardia
- Hyperventilation
- Epigastric tenderness
Identify appropriate investigations for aspirin overdose and interpret the results
• Bloods o Salicylate levels o FBC o U&Es - check for hypokalaemia o LFTs - high AST/ALT o Clotting screen - high PT o Other drug levels (e.g. paracetamol) o ABG - may show mixed metabolic acidosis and respiratory alkalosis • ECG o Signs of hypokalaemia - flattened/inverted T waves, U waves, prolonged PR interval, ST depression
Define asthma
• Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
Explain the aetiology / risk factors of asthma
Genetic Factors o Family history o Atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens) Environmental Factors o House dust mites o Pollen o Pets o Cigarette smoke o Viral respiratory tract infections o Aspergillus fumigatus spores o Occupational allergens
Summarise the epidemiology of asthma
- Affects 10% of children
- Affects 5% of adults
- Prevalence appears to be increasing
Recognise the presenting symptoms of asthma
• Episodic history • Wheeze • Breathlessness • Cough (worse in the morning and at night) IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma Precipitating Factors o Cold o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise o Emotions Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
Recognise the signs of asthma on physical examination
• Tachypnoea • Use of accessory muscles • Prolonged expiratory phase • Polyphonic wheeze • Hyperinflated chest Severe Attack o PEFR < 50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences Life-Threatening Attack o PEFR < 33% predicted o Silent chest o Cyanosis o Bradycardia o Hypotension o Confusion o Coma
Identify appropriate investigations for asthma and interpret the results
ACUTE o Peak flow o Pulse oximetry o ABG o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures CHRONIC o Peak flow monitoring - often shows diurnal variation with a dip in the morning o Pulmonary function test o Bloods - check: • Eosinophilia • IgE level • Aspergillus antibody titres o Skin prick tests - helps identify allergens
Generate a management plan for asthma
ACUTE
o ABCDE
o Resuscitate
o Monitor O2 sats, ABG and PEFR
o High-flow oxygen
o Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly)
o Ipratropium bromide (0.5 mg QDS)
o Steroid therapy
• 100-200 mg IV hydrocortisone
• Followed by, 40 mg oral prednisolone for 5-7 days
o If no improvement –> IV magnesium sulphate
o Consider IV aminophylline infusion
o Consider IV salbutamol
o Anaesthetic help may be needed if the patient is getting exhausted
o IMPORANT: a normal PCO2 is a BAD SIGN in a patient having an asthma attack
• This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low
• A normal PCO2 suggests that the patient is fatiguing
o Treat underlying cause (e.g. infection)
o Give antibiotics if it is an infective exacerbation
o Monitor electrolytes closely because bronchodilators and aminophylline causes a drop in K+
o Invasive ventilation may be needed in severe attacks
o DISCHARGE when:
• PEF > 75% predicted
• Diurnal variation < 25%
• Inhaler technique checked
• Stable on discharge medication for 24 hours
• Patient owns a PEF meter
• Patient has steroid and bronchodilator therapy
• Arrange follow-up
CHRONIC THERAPY
o Start on the step that matches the severity of the patient’s asthma
o STEP 1
• Inhaled short-acting beta-2 agonist used as needed
• If needed > 1/day then move onto step 2
o STEP 2
• Step 1 + regular inhaled low-dose steroids (400 mcg/day)
o STEP 3
• Step 2 + inhaled long-acting beta-2 agonist (LABA)
• If inadequate control with LABA, increase steroid dose (800 mcg/day)
• If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)
o STEP 4
• Increase inhaled steroid dose (2000 mcg/day)
• Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet)
o STEP 5
• Add regular oral steroids
• Maintain high-dose oral steroids
• Refer to specialist care
• Advice
o Teach proper inhaler technique
o Explain important of PEFR monitoring
o Avoid provoking factors
Identify the possible complications of asthma and its management
- Growth retardation
- Chest wall deformity (e.g. pigeon chest)
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
Summarise the prognosis for patients with asthma
- Many children improve as they grow older
* Adult-onset asthma is usually chronic
Define blood product transfusion (incl. red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate)
An injection of a volume of blood product, previously taken from a healthy person, into a patient.
Summarise the indications for a blood product transfusion (incl. red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate)
Red blood cell transfusions are used to treat hemorrhage and to improve oxygen delivery to tissues. Transfusion of red blood cells should be based on the patient’s clinical condition. Indications for transfusion include symptomatic anemia (causing shortness of breath, dizziness, congestive heart failure, and decreased exercise tolerance), acute sickle cell crisis, and acute blood loss of more than 30 percent of blood volume. Fresh frozen plasma infusion can be used for reversal of anticoagulant effects. Platelet transfusion is indicated to prevent hemorrhage in patients with thrombocytopenia or platelet function defects. Cryoprecipitate is used in cases of hypofibrinogenemia, which most often occurs in the setting of massive hemorrhage or consumptive coagulopathy.
Identify the possible complications of a blood product transfusion (incl. red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate)
Transfusion-related infections are less common than noninfectious complications. All noninfectious complications of transfusion are classified as noninfectious serious hazards of transfusion. Acute complications occur within minutes to 24 hours of the transfusion, whereas delayed complications may develop days, months, or even years later.
Identify the possible complications of a blood product transfusion (incl. red cell, platelet, fresh frozen plasma, cryoprecipitate, prothrombin complex concentrate)
HIV, Infection, Cancer, Incompatibility Reaction
Define burns injury
When tissue damage occurs by thermal, electrical or chemical injury
Explain the aetiology / risk factors of burns injury
• Contact with hot objects (lol) • Electricity • UV light • Irradiation • Chemicals High Risk Patients o Young children o Elderly
Summarise the epidemiology of burns injury
UK has > 12,000 admission per year
Recognise the presenting symptoms of burns injury
Note the circumstances of the burn
Important to find out the time, temperature and length of contact with the agent
Consider risk of smoke inhalation and carbon monoxide poisoning
Recognise the signs of burns injury on physical examination
Check for inhalational injury or airway compromise:
o Stridor
o Dyspnoea
o Hoarse voice
o Soot in nose
o Singed nose hairs
o Carbonaceous sputum
Check site, depth and distribution of burn
Partial Thickness Burn
o Subdivided into:
Superficial: red and oedematous skin + PAINFUL
Heals within around 7 days with peeling of dead skin
Deep: blistering and mottling + PAINFUL
Heals over 3 weeks, usually without scarring
Full Thickness Burn
o Destruction of the epidermis and dermis
o Charred leathery eschars
o Firm and PAINLESS with loss of sensation
o Healing will occur by scarring or contractures and requires skin grafting
• Size of Burn
o Described as a percentage of body surface area
Identify appropriate investigations for burns injury and interpret the results
Bloods o Oxygen saturation, ABG and carboxyhaemoglobin (if inhalational injury) o FBC o U&Es o Group and Save Investigations for electrical burns o Serum CK o Urine myoglobin (check for muscle damage) o ECG
Define cardiac arrest
Acute cessation of cardiac function
Explain the aetiology / risk factors of cardiac arrest
The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts FOUR Hs o Hypothermia o Hypoxia o Hypovolaemia o Hypokalaemia/Hyperkalaemia FOUR Ts o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis)) o Thromboembolic o Tamponade o Tension pneumothorax
Summarise the epidemiology of cardiac arrest
None available
Recognise the presenting symptoms of cardiac arrest
- Management precedes or is concurrent to history
* Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness
Recognise the signs of cardiac arrest on physical examination
- Unconscious
- Not breathing
- Absent carotid pulses
Identify appropriate investigations for cardiac arrest and interpret the results
Cardiac Monitor o Allows classification of the rhythm Bloods o ABG o U&E o FBC o X-match o Clotting o Toxicology screen o Blood glucose
Generate a management plan for cardiac arrest
SAFETY IS IMPORTANT
o Approach any arrest scene with caution
o The cause of the arrest may pose a threat
o Defibrillators and oxygen are hazards
Basic Life Support
o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist)
o Clear and maintain the airway with head tilt, jaw thrust and chin lift
o Assess breathing by look, listen and feel
• If they are not breathing, give two rescue breaths
o Assess circulation at carotid pulse for 10 seconds
• If absent - give 30 chest compressions at around 100/min
• Continue cycle of 30 chest compressions for every 2 rescue breaths
o Proceed to advanced life support as soon as possible
Advanced Life Support
o Attach cardiac monitor and defibrillator
o Assess rhythm
• If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)
Defibrillate once (150-360 J biphasic, 360 J monophasic)
• Make sure no one is touching the patient or the bed
Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF
Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins
If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
• If pulseless electrical activity (PEA) or asystole (non-shockable rhythms)
CPR for 2, and then reassess rhythm
Administer adrenaline (1 mg IV) every 3-5 mins
Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm
o During CPR:
• Check electrodes, paddle positions and contacts
• Secure airway
Once secure, give continuous compressions and breaths
• Consider magnesium, bicarbonate and external pacing
• Stop CPR and check pulse only if change in rhythm or signs of life
Treatment of REVERSIBLE causes
o Hypothermia - warm slowly
o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels
o Hypovolaemia - IV colloids, crystalloids and blood products
o Tamponade - pericardiocentesis
o Tension Pneumothorax - aspiration or chest drain
o Thromboembolism - treat as PE or MI
o Toxins - use antidote for given toxin
Identify the possible complications of cardiac arrest and its management
- Irreversible hypoxic brain damage
* Death
Summarise the prognosis for patients with cardiac arrest
- Resuscitation is less successful if cardiac arrest happens outside the hospital
- Increased duration of inadequate effective cardiac output –> poor prognosis
Define cardiac failure (acute and chronic)
• Inability of the cardiac output to meet the body’s demands despite normal venous pressures
Explain the aetiology / risk factors of cardiac failure (acute and chronic)
LOW OUTPUT Cardiac Failure (reduced cardiac output) o Left Heart Failure • Ischaemic heart disease • Hypertension • Cardiomyopathy • Aortic valve disease • Mitral regurgitation o Right Heart Failure • Secondary to left heart failure (in which case it is called congestive cardiac failure) • Infarction • Cardiomyopathy • Pulmonary hypertension/embolus/valve disease • Chronic lung disease • Tricuspid regurgitation • Constrictive pericarditis/pericardial tamponade o Biventricular Failure • Arrhythmia • Cardiomyopathy (dilated or restrictive) • Myocarditis • Drug toxicity HIGH OUTPUT Cardiac Failure (increased demand) o Anaemia o Beri beri o Pregnancy o Paget's disease o Hyperthyroidism o Arteriovenous malformation
