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
Summarise the epidemiology of cardiac failure (acute and chronic)
• 10% > 65 yrs old
Recognise the presenting symptoms of cardiac failure (acute and chronic)
Left Heart Failure - symptoms caused by pulmonary congestion o Dyspnoea - divided based on the New York Heart Association classification: • 1 - no dyspnoea • 2 - dyspnoea on ordinary activities • 3 - dyspnoea on less than ordinary activities • 4 - dyspnoea at rest o Orthopnoea o Paroxysmal nocturnal dyspnoea o Fatigue Acute Left Ventricular Failure o Dyspnoea o Wheeze o Cough o Pink frothy sputum Right Heart Failure o Swollen ankles o Fatigue o Increased weight (due to oedema) o Reduced exercise tolerance o Anorexia o Nausea
Recognise the signs of cardiac failure (acute and chronic) on physical examination
• Left Heart Failure
o Tachycardia
o Tachypnoea
o Displaced apex beat
o Bilateral basal crackles
o S3 gallop (caused by rapid ventricular filling)
o Pansystolic murmur (due to functional mitral regurgitation)
• Acute Left Ventricular Failure
o Tachypnoea
o Cyanosis
o Tachycardia
o Peripheral shutdown
o Pulsus alternans
• Arterial pulse waveforms showing alternating strong and weak beats
• Sign of left ventricular systolic impairment
• Explanation:
In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume
This causes an increase in end-diastolic volume
This means that the left ventricle is stretched more for the next contraction
Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction
This results in a stronger systolic pulse
o Gallop rhythm
o Wheeze (cardiac asthma)
o Fine crackles throughout lung
• Right Heart Failure
o Raised JVP
o Hepatomegaly
o Ascites
o Ankle/sacral pitting oedema
o Signs of functional tricuspid regurgitation
Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results
Bloods o FBC o U&E o LFTs o CRP o Glucose o Lipids o TFTs In ACUTE Left Ventricular Failure o ABG o Troponin o BNP • Raised plasma BNP suggests diagnosis of cardiac failure • Low plasma BNP rules out cardiac failure (90% sensitivity) CXR o Alveolar shadowing o Kerley B lines o Cardiomegaly o Upper Lobe Diversion o Pleural Effusion ECG o May be normal o May show ischaemic changes (pathological q waves, t wave inversion) o May show arrhythmia or left ventricular hypertrophy Echocardiogram o Assess ventricular contraction o Systolic dysfunction = LV ejection fraction < 40% o Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect Swan-Ganz Catheter o Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
Generate a management plan for cardiac failure (acute and chronic)
• Acute Left Ventricular Failure
o Treating Cardiogenic Shock:
• This is severe cardiac failure with low blood pressure
• Requires the use of inotropes (e.g. dobutamine)
• Managed in ITU
o Treating Pulmonary Oedema:
• Sit the patient up
• 60-100% Oxygen (and consider CPAP)
• Diamorphine (venodilator + anxiolytic)
• GTN infusion (venodilator –> reduced preload)
• IV furosemide (venodilator and later diuretic effect)
• Monitor:
BP
Respiratory rate
Oxygen saturation
Urine output
ECG
• TREAT THE CAUSE! (e.g. MI, arrhythmia)
• Chronic Left Ventricular Failure
o TREAT THE CAUSE (e.g. hypertension)
o TREAT EXACERBATING FACTORS (e.g. anaemia)
o ACE Inhibitors
• Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
• They slow down the progression of heart failure and improve survival
o Beta-Blockers
• Blocks the effects of a chronically activated sympathetic system
• Slows progression of heart failure and improves survival
• The benefits of ACE inhibitors and beta-blockers are additive
o Loop Diuretics
• Alongside dietary salt restriction, can correct fluid overload
o Aldosterone Antagonists
• Improves survival in patients with NYHA class III/IV symptoms on standard therapy
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Angiotensin Receptor Blockers
• May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Hydralazine and a Nitrate
• May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers
o Digoxin
• Positive inotrope
• Reduces hospitalisation but does NOT improve survival
o N-3 Polyunsaturated Fatty Acids
• Provide a small beneficial advantage in terms of survival
o Cardiac Resynchronisation Therapy
• Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms
• These patients are also candidates for implantable cardioverter defibrillator (ICD)
• They may receive a combined device
o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)
Identify the possible complications of cardiac failure (acute and chronic) and its management
- Respiratory failure
- Cardiogenic shock
- Death
Summarise the prognosis for patients with cardiac failure (acute and chronic)
• 50% with cardiac failure die within 2 years
Define chronic obstructive pulmonary disease (COPD)
Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
Chronic Bronchitis - Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years.
Emphysema - Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.
Explain the aetiology / risk factors of chronic obstructive pulmonary disease (COPD)
Bronchial and alveolar damage is caused by environmental toxins (e.g. cigarette smoke)
RARE CAUSE: a1 antitrypsin deficiency
Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accomopanying symptoms of cirrhosis)
Chronic Bronchitis
Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis)
Bronchial mucosal oedema
Mucous hypersecretion
Squamous metaplasia
Emphysema
Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1cm)
Summarise the epidemiology of chronic obstructive pulmonary disease (COPD)
Very Common (8% prevalence) Presents in middle age or later More common in males - this may change because there has been a rise in female smokers
Recognise the presenting symptoms of chronic obstructive pulmonary disease (COPD)
Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance
Recognise the signs of chronic obstructive pulmonary disease (COPD) on physical examination
Inspection Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis Percussion Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quient breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions. Sometimes crepitations Signs of CO2 retention Bounding pulse Warm peripheries Asterixis LATE STAGES: signs of right heart failure (cor pulmonale) Right ventricular heave Raised JVP Ankle oedema
Identify appropriate investigations for chronic obstructive pulmonary disease (COPD) and interpret the results
Spirometry and Pulmonary Function Tests
Shows obstructive picture
Reduced PEFR
Reduced FEV1/FVC
Increased lung volumes
Decreased carbon monoxide gas transfer coefficient
CXR
May appear NORMAL
Hyperinflation (> 6 anterior ribs, flattened diaphragm)
Reduced peripheral lung markings
Elongated cardiac silhouette
Bloods
FBC - increased Hb and haematocrit due to secondary polycythaemia
ABG - may show hypoxia, normal/raised PCO2
ECG and Echocardiogram
check for cor pulmonale
Sputum and Blood Cultures - useful in acute infective exacerbations
a1 antitrypsin levels - useful in young patients who have never smoked
Generate a management plan for chronic obstructive pulmonary disease (COPD)
STOP SMOKING
Bronchodilators
Short acting beta 2 agonists (e.g. salbutamol)
Anticholinergics (e.g. ipratropium bromide)
Long acting beta 2 agonists (if > 2 exacerbations per year)
Steroids
Inhaled beclamethasone considered in all patients with FEV1 < 50% of predicted
OR
> 2 exacerbations per year
Regular oral steroids should be avoided if possible
Pulmonary rehabilitation
Oxygen therapy
Only for those who stop smoking
Indicated if:
PaO2 < 7.3 kPa on air during a period of clinical stability
PaO2: 7.3 - 8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
Treatment of Acute Exacerbations
24 % O2 via Venturi mask
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection
Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases
Prevention of infective exacerbations: pneumococcal and influenza vaccination
Identify the possible complications of chronic obstructive pulmonary disease (COPD) and its management
Acute respiratory failure Infections Pulmonary hypertension Right heart failure Pneumothorax (secondary to bullae rupture) Secondary polycythaemia
Summarise the prognosis for patients with chronic obstructive pulmonary disease (COPD)
High morbidity 3 year survival of 90% if < 60 yrs, FEV1 > 50% predicted 3 year survival of 75% if > 60 yrs, FEV1: 40 - 49% predicted
Define diabetic ketoacidosis
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones.
The condition develops when your body can’t produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated.
Explain the aetiology / risk factors of diabetic ketoacidosis
The risk of diabetic ketoacidosis is highest if you:
Have type 1 diabetes
Frequently miss insulin doses
Stress of intercurrent illness
Common cause is omission of insulin because the patient feels unable to eat owing to nausea/vomiting
Uncommonly, diabetic ketoacidosis can occur if you have type 2 diabetes. In some cases, diabetic ketoacidosis may be the first sign that a person has diabetes.
Summarise the epidemiology of diabetic ketoacidosis
0-128 per 1000 people. Prevalence decreased with increasing age. High prevalence in women, non-whites and patients treated with insulin injections
Recognise the presenting symptoms of diabetic ketoacidosis
Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include:
High blood sugar level (hyperglycemia)
High ketone levels in your urine
Recognise the signs of diabetic ketoacidosis on physical examination
Ill appearance Dry skin Labored respiration Dry mucous membranes Decreased skin turgor Decreased reflexes Characteristic acetone (ketotic) breath odor
Effects on vital signs that are related to DKA may include the following: Tachycardia Hypotension Tachypnea Hypothermia Fever, if infection is present
Specific signs of DKA may include the following:
Confusion
Coma
Abdominal tenderness
Identify appropriate investigations for diabetic ketoacidosis and interpret the results
Capillary blood glucose (remember to send a plasma glucose also).
Urine dipstick testing shows marked glycosuria and ketonuria (also send urine for microscopy and culture).
Assay of blood ketones is more sensitive and specific in detecting ketonaemia but is not always available.
Blood tests:
Plasma glucose will be elevated.
FBC - raised WCC is often seen but this does not necessarily indicate sepsis, as it may occur in DKA.
Electrolytes - Na+ may be high due to dehydration, low due to interference of glucose/ketones with assay, or normal; K+ may be high due to the effect of acidosis, normal or occasionally low but overall there is cell depletion of K+.
Urea and creatinine - elevated due to prerenal acute kidney injury or where renal impairment is the primary cause.
Arterial blood gases - metabolic acidosis with low pH and low HCO3; pCO2 should be normal but can be depressed by respiratory compensation; low pO2 may indicate a primary respiratory problem as a precipitant.
Cardiac enzymes - if myocardial ischaemia/infarction is suspected - eg, troponin.
Creatine kinase - rhabdomyolysis may also exist (also increased in myocardial infarction).
Amylase - if pancreatitis is suspected.
Blood cultures.
12-lead ECG.
CXR.
Abdominal X-ray - if indicated by history and examination.
CT/MRI scan of the head - if there is impairment of consciousness or focal neurology.
Lumbar puncture - may be indicated if meningitis is a possible precipitant.
Generate a management plan for diabetic ketoacidosis
• Replace fluid losses with normal saline
• Replace electrolyte losses:
o Potassium levels need to be monitored with great care
o Patients have a total body potassium deficit although initial plasma levels may not be low
o Insulin therapy leads to uptake of potassium by the cells with a consequent fall in plasma levels
o Potassium is, therefore, given as soon as insulin therapy is started
• Restore the acid-base balance:
o A patient with healthy kidneys will rapidly compensate for the metabolic acidosis once the circulating volume is restored
o Only consider bicarbonate if the pH is < 7
• Administer insulin:
o Soluble insulin is given as an IV infusion where facilities for adequate supervision exist, otherwise as hourly IM injections
o Do not give subcutaneously as the peripheral blood flow is reduced in a shocked patient
• Monitor blood glucose closely
• Replace the energy losses
• Seek the underlying cause (especially infection)
Identify the possible complications of diabetic ketoacidosis and its management
Problems of management:
• Hypotension:
o This may lead to renal failure. Give plasma expanders or whole blood if systolic BP < 80mmHg
• Coma:
o It is essential to pass a NG tube to prevent a drowsy patient aspirating when vomiting
• Cerebral oedema:
o Rare and believed to be due to excessive rehydration.
High mortality
• Hypothermia:
o Monitor patient’s temperature rectally to avoid this
• Late complications (e.g. stasis pneumonia and DVT)
Summarise the prognosis for patients with diabetic ketoacidosis
Mortality rates have fallen significantly in a period of 20 years - from 7.96% to 0.67%. The mortality rate is still high in developing countries and among non-hospitalised patients.
Prognosis worsens with age and the nature and severity of the underlying precipitating pathology (particularly myocardial infarction, sepsis and pneumonia).
The presence of coma at presentation, hypothermia or persistent oliguria are poor prognostic indicators.
Cerebral oedema remains the most common cause of mortality, particularly in young children and adolescents.
The main causes of mortality in the adult population include severe hypokalaemia, adult respiratory distress syndrome and comorbid states such as pneumonia, acute myocardial infarction and sepsis.
Define disseminated intravascular coagulation (DIC)
• A disorder of the clotting cascade that can complicate a serious illness.
DIC can occur in TWO forms:
• Acute overt form where there is bleeding and depletion of platelets and clotting factors
• Chronic non-overt form where thromboembolism is accompanied by generalised activation of the coagulation system
Explain the aetiology / risk factors of disseminated intravascular coagulation (DIC)
Infection - particularly GRAM-NEGATIVE sepsis
Obstetric Complications
o Missed miscarriage (when the foetus dies but the body doesn’t realise it and the placenta continues to release hormones)
o Severe pre-eclampsia
o Placental abruption (separation of the placenta from the wall of the uterus during pregnancy)
o Amniotic emboli
Malignancy
o Acute promyelocytic leukaemia - ACUTE DIC
o Lung, breast and GI malignancy - CHRONIC DIC
Severe trauma or surgery
Others: haemolytic transfusion reaction, burns, severe liver disease, aortic aneurysms, haemangiomas
Pathophysiology
Acute DIC
• Endothelial damage and the release of granulocyte/macrophage procoagulant substances (e.g. tissue factor) lead to activation of coagulation
• This leads to explosive thrombin generation, which depletes clotting factors and platelets, whilst also activating the fibrinolytic system
• This leads to bleeding in the subcutaneous tissues, skin and mucous membranes
• Occlusion of blood vessels by fibrin in the microcirculation leads to microangiopathic haemolytic anaemia and ischaemic organ damage
Chronic DIC
• IDENTICAL process to acute DI
• Happens at a slower rate with time for compensatory responses
• The compensatory responses diminish the likelihood of bleeding but give rise to hypercoagulable states and thrombosis can occur
Summarise the epidemiology of disseminated intravascular coagulation (DIC)
• Seen in any severely ill patient
Recognise the presenting symptoms of disseminated intravascular coagulation (DIC)
- The patients will tend to be severely unwell with symptoms of the underlying disease
- Confusion
- Dyspnoea
- Evidence of bleeding
Recognise the signs of disseminated intravascular coagulation (DIC) on physical examination
Signs of underlying disease
Fever
Evidence of shock (hypotension, tachycardia)
Acute DIC o Petechiae, purpura, ecchymoses o Epistaxis o Mucosal bleeding o Overt haemorrhage o Signs of end organ damage o Respiratory distress o Oliguria due to renal failure
Chronic DIC
o Signs of deep vein and arterial thrombosis or embolism
o Superficial venous thrombosis
Identify appropriate investigations for disseminated intravascular coagulation (DIC) and interpret the results
Bloods o FBC • Low platelets • Low Hb • High APTT/PT • Low fibrinogen • High fibrin degradation products • High D-dimers Peripheral Blood Film o Schistocytes
Define encephalitis
• Inflammation of the brain parenchyma
Explain the aetiology / risk factors of encephalitis
Most commonly due to VIRAL INFECTION Viral Causes o Herpes Simplex Virus - MOST COMMON in the UK o VZV o Mumps o Adenovirus o Coxsackie o EBV o HIV o Japanese encephalitis Non-Viral (RARE) o Syphilis o Staphylococcus aureus In immunocompromised patients o CMV o Toxoplasmosis o Listeria Autoimmune or Paraneoplastic o Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)
Summarise the epidemiology of encephalitis
• UK incidence: 7.4/100,000
Recognise the presenting symptoms of encephalitis
- In most cases, encephalitis is self-limiting and mild
- Subacute onset (hours to days)
- Headache
- Fever
- Vomiting
- Neck stiffness
- Photophobia
- Behavioural changes
- Drowsiness
- Confusion
- History of seizures
- Focal neurological symptoms (e.g. dysphagia, hemiplegia)
- Obtain a detailed TRAVEL HISTORY
Recognise the signs of encephalitis on physical examination
- Reduce consciousness
- Deteriorating GCS
- Seizures
- Pyrexia
Signs of Meningism:
o Neck stiffness
o Photophobia
o Kernig’s test positive
Signs of raised ICP:
o Cushing’s Response: hypertension + bradycardia + irregular breathing
o Papilloedema
Focal neurological signs
MMSE may reveal cognitive/psychiatric disturbance
Identify appropriate investigations for encephalitis and interpret the results
Bloods o FBC - high lymphocytes (indicates viral cause) o U&Es - SIADH may occur as a result of encephalitis o Glucose o Viral serology o ABG MRI/CT o Exclude mass lesion o HSV causes oedema of the temporal lobe on MRI Lumbar Puncture o High lymphocytes o High monocytes o High protein o Glucose is usually normal o Viral PCR EEG - may show epileptiform activity Brain biopsy (rarely needed)
Define epidural
Epidural administration is a medical route of administration in which a drug such as epidural analgesia and epidural anaesthesia or contrast agent is injected into the epidural space around the spinal cord.
Summarise the indications for an epidural
during childbirth, including caesareans
during some types of surgery
after some types of surgery
Steroid medication can also be given as an epidural injection to treat back or leg pain caused by sciatica or a slipped (prolapsed) disc.
Identify the possible complications of an epidural
low blood pressure, which can make you feel lightheaded or nauseous temporary loss of bladder control itchy skin feeling sick headaches nerve damage
Define epilepsy
- A tendency to recurrent unprovoked seizures
- You need to have had > 2 seizures for epilepsy to be diagnosed
Definition of Seizure: paroxysmal synchronised cortical electrical discharges
Types of Seizure
Focal Seizure: seizure localised to specific cortical regions (e.g. temporal lobe seizure). These can be further divided into:
• COMPLEX partial seizure: consciousness is affected
• SIMPLE partial seizure: consciousness is NOT affected
Generalised Seizure: seizures that affect the whole of the brain. It also affects consciousness. There are different types of generalised seizure:
• Tonic-clonic
• Absence
• Myoclonic
• Atonic
• Tonic
Explain the aetiology / risk factors of epilepsy
Most cases are IDIOPATHIC
Primary epilepsy syndromes (e.g. idiopathic generalised epilepsy)
Secondary Seizures
o Tumour
o Infection (e.g. meningitis)
o Inflammation (e.g. vasculitis)
o Toxic/Metabolic (e.g. sodium imbalance)
o Drugs (e.g. alcohol withdrawal)
o Vascular (e.g. haemorrhage)
o Congenital abnormalities (e.g. cortical dysplasia)
o Neurodegenerative disease (e.g. Alzheimer’s disease)
o Malignant hypertension or eclampsia
o Trauma
Common things that look like seizures
o Syncope
o Migraine
o Non-epileptiform seizure disorder (e.g. dissociative disorder)
Pathophysiology of Seizures
o Result from an imbalance in the inhibitory and excitatory currents or neurotransmission in the brain
o Precipitants include anything that promotes excitation of the cerebral cortex
o Often it is unclear why the precipitants cause seizures
Summarise the epidemiology of epilepsy
- COMMON
- 1% of the general population
- Typical age of onset: CHILDREN and ELDERLY
Recognise the presenting symptoms of epilepsy
Try and obtain a collateral history from a witness as well as the patient
Key features to consider when taking a history from a potential epilepsy patient:
o Rapidity of onset
o Duration of episode
o Any alteration in consciousness?
o Any tongue-biting or incontinence?
o Any rhythmic synchronous limb jerking?
o Any post-ictal abnormalities (e.g. exhaustion, confusion)?
o Drug history (alcohol, recreational drugs)
Focal Seizure Presentation
o Frontal Lobe Focal Motor Seizure
• Motor convulsions
• May show a Jacksonian march (when the muscular spasm caused by the simple partial seizure spreads from affecting the distal part of the limb towards the ipsilateral face)
• May show post-ictal flaccid weakness (Todd’s paralysis)
Temporal Lobe Seizures
• Aura (visceral or psychic symptoms)
• Hallucinations (usually olfactory or affecting taste)
Frontal Lobe Complex Partial Seizure • Loss of consciousness • Involuntary actions/disinhibition • Rapid recovery • Generalised Seizures
Tonic-Clonic (Grand Mal)
• Vague symptoms before attack (e.g. irritability)
• Tonic phase (generalised muscle spasm)
• Clonic phase (repetitive synchronous jerks)
• Faecal/urinary incontinence
• Tongue biting
• Post-ictal phase: impaired consciousness, lethargy, confusion, headache, back pain, stiffness
Absence (Petit Mal)
• Onset in CHILDHOOD
• Loss of consciousness but MAINTAINTED POSTURE
• The patient will appear to stop talking and stare into space for a few seconds
• NO post-ictal phase
Non-Convulsive Status Epilepticus
• Acute confusional state
• Often fluctuating
• Difficult to distinguish from dementia
Recognise the signs of epilepsy on physical examination
- Depends on aetiology
* Patients tend to be normal in between seizures
Identify appropriate investigations for epilepsy and interpret the results
Bloods o FBC o U&E o LFTs o Glucose o Calcium o Magnesium o ABG o Toxicology screen o Prolactin - shows a transient increase shortly after seizures
EEG
o Helps to confirm diagnosis
o Helps classify the epilepsy
o Ictal EEGs are particularly useful (i.e. during a seizure)
CT/MRI
o Shows structural, space-occupying or vascular lesions
Other investigations
o If it is suspected to be a secondary seizure (e.g. due to infection)
Generate a management plan for epilepsy
Treatment of STATUS EPILEPTICUS
DEFINITION of Status Epilepticus: a seizure lasting > 30 mins or repeated seizure without recovery and regain of consciousness in between
o Although the definition states that the seizure must last > 30 mins, treatment is usually initiated early (after around 5-10 mins)
o ABC approach
o Check GLUCOSE (give glucose if hypoglycaemic)
o IV lorazepam OR IV/PR diazepam - REPEAT again after 10 mins if seizure does not terminate
o If seizures recur following the next dose of lorazepam or diazepam, consider IV phenytoin - an ECG monitor is required
NOTE: other agents include phenobarbitone, levetiracetam and sodium valproate
o If this also fails, consider general anaesthesia (e.g. thiopentone) - intubation and mechanical ventilation required
o Treat the CAUSE (e.g. hypoglycaemia or hyponatraemia)
o Check plasma levels of anticonvulsants (because status epilepticus is often caused by lack of compliance with anti-epileptic medications)
Treatment of newly diagnosed epilepsy
o Only start anti-convulsant treatment after > 2 unprovoked seizures
o FOCAL Seizure 1st Line: lamotrigine or carbamazepine
o GENERALISED Seizure 1st Line: sodium valproate
o Start treatment with only ONE anti-epileptic drug
o Other anti-convulsants: phenytoin, levetiracetam, clobazam, topiramate, gabapentin, vigabatrin
Patient Education
o Avoid triggers
o Use seizure diaries
o Particular consideration for women of child-bearing age because the anti-epileptic drugs can have teratogenic effects
o Be careful of drug interactions (e.g. AEDs can reduce the effectiveness of the oral contraceptive pill)
Surgery may be considered for refractory epilepsy
Identify the possible complications of epilepsy (incl. status epilepticus) and its management
• Fractures from tonic-clonic seizures • Behavioural problems • Sudden death in epilepsy (SUDEP) • Complications of anti-epileptic drugs: o Gingival hypertrophy (phenytoin) o Neutropaenia and osteoporosis (carbamazepine) o Stevens-Johnson syndrome (lamotrigine)
Summarise the prognosis for patients with epilepsy
• 50% remission at 1 year
Define extradural haemorrhage
• Bleeding and accumulation of blood in the extradural space
Explain the aetiology / risk factors of extradural haemorrhage
TRAUMA
o Usually due to fracture of the temporal or parietal bones leading to rupture of the middle meningeal artery
Risk Factors
o Bleeding tendency
• E.g. haemophilia, anticoagulant therapy
Summarise the epidemiology of extradural haemorrhage
- UK incidence: 20/10,000
- 10% of severe head injuries
- Most commonly seen in YOUNG ADULTS
Recognise the signs of extradural haemorrhage on physical examination
- Head injury with temporary loss of consciousness
- Followed by lucid interval
- Followed by progressive deterioration in conscious level
Recognise the presenting symptoms of extradural haemorrhage
• Scalp trauma or fracture • Headache • Deteriorating GCS Signs of raised ICP o E.g. dilated, unresponsive pupil on the side of the injury Cushing's Reflex o Hypertension o Bradycardia o Irregular breathing
Identify appropriate investigations for extradural haemorrhage and interpret the results
• Urgent CT Scan
o Check for a haematoma
o Look for features of raised ICP (e.g. midline shift)
Define head injury
Traumatic brain injury usually results from a violent blow or jolt to the head or body. An object that penetrates brain tissue, such as a bullet or shattered piece of skull, also can cause traumatic brain injury.
Mild traumatic brain injury may affect your brain cells temporarily. More-serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain. These injuries can result in long-term complications or death.
Explain the aetiology / risk factors of head injury
Children, especially newborns to 4-year-olds
Young adults, especially those between ages 15 and 24
Adults age 60 and older
Males in any age group
Recognise the presenting symptoms of head injury
Mild traumatic brain injury
The signs and symptoms of mild traumatic brain injury may include:
Physical symptoms Loss of consciousness for a few seconds to a few minutes No loss of consciousness, but a state of being dazed, confused or disoriented Headache Nausea or vomiting Fatigue or drowsiness Problems with speech Difficulty sleeping Sleeping more than usual Dizziness or loss of balance
Sensory symptoms Sensory problems, such as blurred vision, ringing in the ears, a bad taste in the mouth or changes in the ability to smell Sensitivity to light or sound Cognitive or mental symptoms Memory or concentration problems Mood changes or mood swings Feeling depressed or anxious
Moderate to severe traumatic brain injuries
Moderate to severe traumatic brain injuries can include any of the signs and symptoms of mild injury, as well as these symptoms that may appear within the first hours to days after a head injury:
Physical symptoms
Loss of consciousness from several minutes to hours
Persistent headache or headache that worsens
Repeated vomiting or nausea
Convulsions or seizures
Dilation of one or both pupils of the eyes
Clear fluids draining from the nose or ears
Inability to awaken from sleep
Weakness or numbness in fingers and toes
Loss of coordination
Cognitive or mental symptoms
Profound confusion
Agitation, combativeness or other unusual behavior
Slurred speech
Coma and other disorders of consciousness
Children’s symptoms
Infants and young children with brain injuries might not be able to communicate headaches, sensory problems, confusion and similar symptoms. In a child with traumatic brain injury, you may observe:
Change in eating or nursing habits Unusual or easy irritability Persistent crying and inability to be consoled Change in ability to pay attention Change in sleep habits Seizures Sad or depressed mood Drowsiness Loss of interest in favorite toys or activities
Recognise the signs of head injury on physical examination
Loss of consciousness at any time. GCS <15 on initial assessment. Focal neurological deficit. Retrograde or anterograde amnesia. Persistent headache. Vomiting or seizures post injury.
Identify appropriate investigations for head injury and interpret the results
CT Head
MRI Head
Define ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome.
ACS can be further subdivided into:
o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
o NSTEMI
o STEMI - ST elevation with transmural infarction
o NOTE: MI = cardiac muscle necrosis resulting from ischaemia
Explain the aetiology / risk factors of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
- COMMON
- Prevalence: > 2 %
- More common in males
- Annual incidence of MI in the UK ~ 5/1000
Summarise the epidemiology of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
- Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
- This is usually due to atherosclerosis
- Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli
Atherosclerosis pathophysiology
o Endothelial injury leads to migration of monocytes into the subendothelial space
o These monocytes differentiate into macrophages
o Macrophages accumulate LDL lipids and become foam cells
o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans
o This leads to the formation of an atherosclerotic plaque
Risk Factors o Male o Diabetes mellitus o Family history o Hypertension o Hyperlipidaemia o Smoking
Recognise the presenting symptoms of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
ACS
o Acute-onset chest pain
o Central, heavy, tight, crushing pain
o Radiates to the arms, neck, jaw or epigastrium
o Occurs at rest
o More severe and frequent pain that previously occurring stable angina
o Associated symptoms:
• Breathlessness
• Sweating
• Nausea and vomiting
• SILENT INFARCTS occur in the elderly and diabetics
Stable Angina
o Chest pain brought on by exertion and relieved by rest
Recognise the signs of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) on physical examination
Stable Angina
o Check for signs of risk factors
ACS o There may be NO CLINICAL SIGNS o Pale o Sweating o Restless o Low-grade pyrexia o Check both radial pulses to rule out aortic dissection o Arrhythmias o Disturbances of BP o New heart murmurs o Signs of complications (e.g. acute heart failure, cardiogenic shock)
Identify appropriate investigations for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and interpret the results
Bloods o FBC o U&Es o CRP o Glucose o Lipid profile o Cardiac enzymes (troponins and CK-MB) o Amylase (pancreatitis could mimic MI) o TFTs o AST and LDH (raised 24 and 48 hours post-MI, respectively)
ECG o Unstable Angina or NSTEMI: • May show ST depression or T wave inversion o STEMI: • Hyperacute T waves • ST elevation (> 1 mm in limb leads, > 2 mm in chest leads) • New-onset LBBB • Later changes: T wave inversion Pathological Q waves
Relationship between ECG leads and the side of the heart
• Inferior: II, III, aVF
• Anterior: V1-V5/6
• Lateral: I, aVL, V5/6
• Posterior: Tall R wave and ST depression in V1-3
CXR - Check for signs of heart failure
Exercise ECG
Indications
• Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
• Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
• NOTE: digoxin is associated with giving a false-positive result
Results:
Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
NOTE: beta-blockers reduce heart rate and so should be stopped before the test
Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
Radionuclide Myocardial Perfusion Imaging (rMPI)
o Uses Technetium-99m sestamibi or tetrofosmin
o Can be performed under stress or at rest
o Stress testing shows low uptake in ischaemic myocardium
Echocardiogram
o Measures left ventricular ejection fraction
o Exercise or dobutamine stress echo may detect regional wall motion abnormalities
Pharmacological Stress Testing
o This is used in patients who are unable to exercise
o Pharmacological agents can be used to induce a tachycardia, such as:
• Dipyridamole
• Adenosine
• Dobutamine
o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
Cardiac Catheterisation/Angiography
o Performed if ACS with positive troponin or if high risk on stress testing
Coronary Calcium Scoring
o Uses specialised CT scan
o May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia
Generate a management plan for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
STABLE ANGINA
Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
• All patients should receive aspirin 75 mg/day unless contraindicated
Immediate symptom relief (e.g. GTN spray)
Long-term management
Beta-blockers: Contraindicated in:
• Acute heart failure
• Cardiogenic shock
• Bradycardia
• Heart block
• Asthma
Calcium channel blockers
Nitrates
Percutaneous coronary intervention (PCI)
• Performed in patients with stable angina despite maximal tolerable medical therapy
Coronary artery bypass graft (CABG)
• Occurs in more severe cases (e.g. three-vessel disease)
UNSTABLE ANGINA/NSTEMI
o Admit to coronary care unit
o Oxygen, IV access, monitor vital signs and serial ECG
o GTN
o Morphine
o Metoclopramide (to counteract the nausea caused by morphine)
o Aspirin (300 mg initially, followed by 75 mg indefinitely)
o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
o LMWH (e.g. enoxaparin)
o Beta-blocker (e.g. metoprolol)
o Glucose-insulin infusion if blood glucose > 11 mmol/L
o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
• Undergoing PCI
• At high risk of further cardiac events
o If little improvement, consider urgent angiography with/without revascularisation
NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH • Morphine • Oxygen • Nitrates • Anticoagulants (aspirin + clopidogrel) • Beta-blockers • ACE inhibitors • Statins • Heparin
STEMI
o Same as UAP/NSTEMI management except:
• Clopidogrel
600 mg if patient is going to PCI
300 mg if undergoing thrombolysis and < 75 yrs
75 mg if undergoing thrombolysis and > 75 yrs
MAINTENANCE: 75 mg daily for at least 1 year
If undergoing primary PCI:
IV heparin (plus GlpIIb/IIIa inhibitor)
Bivalirudin (antithrombin)
Primary PCI
• Goal < 90 min if available
Thrombolysis
• Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase)
• Only considered if within 12 hours of chest pain with ECG changes and not contraindicated
• Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis
Secondary Prevention • Dual antiplatelet therapy (aspirin + clopidogrel) • Beta-blockers • ACE inhibitors • Statins • Control risk factors
Advice
• No driving for 1 month following MI
CABG
• Considered in patients with left main stem or three-vessel disease
Identify the possible complications of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and its management
- Increased risk of MI and other vascular disease (e.g. stroke, PVD)
- Cardiac injury from an MI can lead to heart failure and arrhythmias
Early Complications (within 24-72 hrs) o Death o Cardiogenic shock o Heart failure o Ventricular arrythmias o Heart block o Pericarditis o Myocardial rupture o Thromboembolism
Late Complications o Ventricular wall rupture o Valvular regurgitation o Ventricular aneurysms o Tamponade o Dressler's syndrome o Thromboembolism
MNEMONIC for Complications of MI o Death o Arrhythmias o Rupture o Tamponade o Heart failure o Valve disease o Aneurysm o Dressler's syndrome o Embolism
Summarise the prognosis for patients with ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)
• TIMI score (0-7) can be used for risk stratification
o NOTE: TIMI = thrombolysis in myocardial infarction
o High scores are associated with high risk of cardiac events within 30 days of MI
Killip Classification of acute MI can also be used:
o Class I: no evidence of heart failure
o Class II: mild to moderate heart failure
o Class III: over pulmonary oedema
o Class IV: cardiogenic shock
Define meningitis
• Inflammation of the leptomeningeal (pia and arachnoid mater) coverings of the brain, most commonly due to infection
Explain the aetiology / risk factors of meningitis
BACTERIAL Neonates • Group B streptococci • Escherichia coli • Listeria monocytogenes Children • Haemophilus influenzae • Neisseria meningitidis • Streptococcus pneumoniae Adults • Neisseria meningitidis • Streptococcus pneumoniae • Tuberculosis Elderly • Streptococcus pneumoniae • Listeria monocytogenes
VIRAL o Enteroviruses o Mumps o HSV o VZV o HIV
Fungal o Cryptococcus (common cause of meningitis in HIV patients)
Others
o Aseptic meningitis (not due to microbes)
o Mollaret’s meningitis (recurrent benign lymphocytic meningitis)
RISK FACTORS o Close communities (e.g. college halls) o Basal skull fractures o Mastoiditis o Sinusitis o Inner ear infections o Alcoholism o Immunodeficiency o Splenectomy o Sickle cell anaemia o CSF shunts o Intracranial surgery
Summarise the epidemiology of meningitis
• UK: 2500 notifications/yr
Recognise the presenting symptoms of meningitis
- Severe headache
- Photophobia
- Neck or backache
- Irritability
- Drowsiness
- Vomiting
- High-pitched crying or fits (common in children)
- Reduced consciousness
- Fever
IMPORTANT: take a good travel history and exposure history and take not of exposure to any of the following
o Rodents (lymphocytic choriomeningitis virus)
o Ticks (Lyme borrelia, Rocky Mountain spotted fever)
o Mosquitoes (West Nile virus)
o Sexual activity (HSV-2, HIV, syphilis)
o Travel
Recognise the signs of meningitis on physical examination
• Signs of MENINGISM
o Photophobia
o Neck stiffness
o Kernig’s Sign - with the hips flexed, there is pain/resistance on passive knee extension
o Brudzinski’s Sign - flexion of the hips when the neck is flexed
• Signs of INFECTION o Fever o Tachycardia o Hypotension o Skin rash o Altered mental state
Identify appropriate investigations for meningitis and interpret the results
Bloods
o Two sets of blood cultures
Imaging
o CT scan - exclude mass lesion or raised ICP before LP
Lumbar Puncture o MC&S o Bacterial meningitis: • Cloudy CSF • High neutrophils • High protein • Low glucose o Viral meningitis: • High lymphocytes • High protein • Normal glucose o TB meningitis: • Fibrinous CSF • High lymphocytes • High protein • Low glucose
Generate a management plan for meningitis
IMMEDIATE IV Antibiotics (before LP)
o First choice: 3rd generation cephalosporin (e.g. cefotaxime or ceftriaxone)
o Benzylpenicillin may be used as an initial blind therapy
Dexamethasone IV
o Given shortly before or with the first dose of antibiotics
o Associated with a reduced risk of complications
Resuscitation
o Manage in ITU
o Notify public health services
Identify the possible complications of meningitis and its management
- Septicaemia
- Shock
- DIC
- Renal failure
- Seizures
- Peripheral gangrene
- Cerebral oedema
- Cranial nerve lesions
- Cerebral venous thrombosis
- Hydrocephalus
- Waterhouse-Friderichsen Syndrome (bilateral adrenal haemorrhage caused by severe meningococcal infection)
Summarise the prognosis for patients with meningitis
- Mortality rate from bacterial meningitis: 10-40% with meningococcal sepsis
- Viral meningitis is self-limiting
Define multi-organ dysfunction syndrome
• A clinical syndrome characterised by the development of progressive and potentially reversible physiologic dysfunction of 2 or more organs or organ systems that is induced by a variety of insults, including sepsis.
Explain the aetiology / risk factors of multi-organ dysfunction syndrome
Usually results from:
o Infection
o Injury
o Hypoperfusion
o Hypermetabolism
• This primary cause can trigger a systemic inflammatory response (sepsis or SIRS)
• MODS is the final stage in a continuum beginning with SIRS + infection:
o SIRS + infection –> sepsis –> severe sepsis –> MODS
Summarise the epidemiology of multi-organ dysfunction syndrome
• Not very common
Recognise the presenting symptoms of multi-organ dysfunction syndrome
Multiple Organ Dysfunction Score
o Stage 1 - increased volume requirements, mild respiratory alkalosis, oliguria, hyperglycaemia, increased insulin requirements
o Stage 2 - tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction and haematologic abnormalities
o Stage 3 - shock, azotaemia (high nitrogen in the blood), acid-base disturbance, significant coagulation abnormalities
o Stage 4 - vasopressor dependent, oliguria or anuria, development of ischaemic colitis and lactic acidosis
Recognise the signs of multi-organ dysfunction syndrome on physical examination
Multiple Organ Dysfunction Score
o Stage 1 - increased volume requirements, mild respiratory alkalosis, oliguria, hyperglycaemia, increased insulin requirements
o Stage 2 - tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction and haematologic abnormalities
o Stage 3 - shock, azotaemia (high nitrogen in the blood), acid-base disturbance, significant coagulation abnormalities
o Stage 4 - vasopressor dependent, oliguria or anuria, development of ischaemic colitis and lactic acidosis
Identify appropriate investigations for multi-organ dysfunction syndrome and interpret the results
- Monitor vital signs
* ABG may be necessary to look at hypoxaemia, lactic acidosis etc.
Define opiate overdose
• Taking more opiates than you should
Explain the aetiology / risk factors of opiate overdose
• Opiates have widespread effects across the body and side-effects can range from constipation to respiratory depression and death • Drugs involved: o Codeine o Diamorphine o Dihydrocodeine o Fentanyl o Loperamide o Methadone o Morphine
Risk Factors o Mental health conditions o Alcoholics Morphine toxicity at a lower dose due to: • Hepatic impairment • Renal impairment • Hypotension • Hypothyroidism • Asthma (decreased respiratory reserve)
Summarise the epidemiology of opiate 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
Recognise the presenting symptoms of opiate overdose
- Constipation (if chronic)
- Nausea and vomiting
- Loss of appetite
- Sedation
- Craving the next dose
- Drowsiness (if acute overdose)
Recognise the signs of opiate overdose on physical examination
- Respiratory depression
- Hypotension and tachycardia
- Pinpoint pupils
Identify appropriate investigations for opiate overdose and interpret the results
- Toxicology screen
- Paracetamol blood level (should be considered in patients who have self-poisoned)
- If in doubt, give a small test dose of naloxone
Define paracetamol overdose
• Excessive ingestion of paracetamol causing toxicity
Explain the aetiology / risk factors of paracetamol overdose
- MAX recommended dose: 2 x 500 mg tablets, 4 x in 24 hrs
- Intake > 12 g can cause hepatic necrosis
Risk Factors
o Chronic alcohol abusers
o Patients on enzyme-inducing drugs (e.g. anticonvulsants)
o Malnourished
o Anorexia nervosa
o HIV
o Paracetamol overdose is commonly associated with ingestion of large amounts of alcohol
Summarise the epidemiology of paracetamol overdose
- Most COMMON intentional drug overdose in the UK
* Causes 100 deaths/yr in the UK
Recognise the presenting symptoms of paracetamol overdose
• Make sure you ascertain the TIMING and QUANTITY of overdose and presence of risk factors
0-24 hrs o ASYMPTOMATIC o Mild nausea/vomiting o Lethargy o Malaise
24-72 hrs
o RUQ pain
o Vomiting
72+ hrs
o Increased confusion (encephalopathy)
o Jaundice
Recognise the signs of paracetamol overdose on physical examination
- 0-24 hrs - no signs
- 24-72 hrs - liver enlargement and tenderness
- 72+ hrs - jaundice, coagulopathy, hypoglycaemia, renal angle tenderness
Identify appropriate investigations for paracetamol overdose and interpret the results
• Measure paracetamol levels
o NOTE: peak paracetamol levels are 4 hrs after ingestion
• Others: FBC, U&Es, Glucose, LFTs, Clotting Screen, Lactate and ABG
Define stroke (ischaemic and haemorrhagic)
• Rapid permanent neurological deficit from cerebrovascular insult. Also defined clinically, as focal or global impairment of CNS function developing rapidly and lasting > 24 hrs
• Can be subdivided based on:
o Location - anterior circulation vs posterior circulation
o Pathological Process - infarction vs haemorrhage
Explain the aetiology / risk factors of stroke (ischaemic and haemorrhagic)
INFARCTION (80%)
Thrombosis
• Can occur in small vessels (lacunar infarcts)
• Can occur in larger vessels (e.g. middle cerebral artery)
• Can arise in prothrombotic states (e.g. dehydration, thrombophilia)
Emboli
• From carotid dissection, carotid atherosclerosis, atrial fibrillation
• NOTE: they can arise from venous blood clots that pass through a septal defect (e.g. VSD) and get lodged in the cerebral circulation
Hypotension
• If the blood pressure is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories
Others
• Vasculitis
• Cocaine (arterial spasm)
HAEMORRHAGE (10%)
o Hypertension
o Charcot-Bouchard microaneurysm rupture (DEFINITION: aneurysms within the brain vasculature that occur in small blood vessels)
o Amyloid angiopathy
o Arteriovenous malformations
o Less common: trauma, tumours, vasculitis
Summarise the epidemiology of stroke (ischaemic and haemorrhagic)
- COMMON
- Incidence: 2/1000
- 3rd most common cause of death in industrialised countries
- Usual age of stroke patients: 70+
Recognise the presenting symptoms of stroke (ischaemic and haemorrhagic)
- SUDDEN-ONSET
- Weakness
- Sensory, visual or cognitive impairment
- Impaired coordination
- Impaired consciousness
- Head or neck pain (if carotid or vertebral artery dissection)
- Enquire about time of onset (critical for emergency management if < 4.5 hrs)
- Enquire about history of AF, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain
Recognise the signs of stroke (ischaemic and haemorrhagic) on physical examination
- Examine for underlying cause (e.g. atrial fibrillation)
- Infarction
Lacunar Infarcts
• Affecting the internal capsule or pons: pure sensory or motor deficit (or both)
• Affecting the thalamus: loss of consciousness, hemisensory deficit
• Affecting the basal ganglia: hemichorea, hemiballismus, parkinsonism
Anterior Circulation
• Anterior Cerebral
Lower limb weakness
Confusion
Middle Cerebral Facial weakness Hemiparesis (motor cortex) Hemisensory loss (sensory cortex) Apraxia Hemineglect (parietal lobe) Receptive or expressive dysphasia (due to involvement of Wernicke's and Broca's areas) Quadrantopia (if superior or inferior optic radiations are affected)
Posterior Circulation
• Posterior Cerebral - hemianopia
• Anterior Inferior Cerebellar - vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness
• Posterior Inferior Cerebellar (affected in lateral medullary syndrome) - vertigo, ipsilateral ataxia, ipsilateral Horner’s syndrome, ipsilateral hemisensory loss, dysarthria, contralateral spinothalamic sensory loss
• Basilar Artery - cranial nerve pathology and impaired consciousness
• Multiple Lacunar Infarcts - vascular dementia, urinary incontinence, gait apraxia, shuffling gait, normal or excessive arm-swing
• Intracerebral - headache, meningism, focal neurological signs, nausea/vomiting, signs of raised ICP, seizures
Identify appropriate investigations for stroke (ischaemic and haemorrhagic) and interpret the results
Bloods
o Clotting profile - check if thrombophilia (especially in young patients)
ECG
o Check for arrhythmias that may be the source of the clot
Echocardiogram
o Identify cardiac thrombus, endocarditis and other cardiac sources of embolism
Carotid Doppler Ultrasound
o Check for carotid artery disease (e.g. atherosclerosis)
CT Head Scan
o Rapid detection of haemorrhages
MRI-Brain
o Higher sensitivity for infarction but less available
CT Cerebral Angiogram
o Detect dissections or intracranial stenosis
Generate a management plan for stroke (ischaemic and haemorrhagic)
HYPERACUTE STROKE
o If < 4.5 hrs from onset
o Exclude haemorrhage using CT-head
o If haemorrhage excluded, thrombolysis may be considered
ACUTE ISCHAEMIC STROKE
o Aspirin + Clopidogrel to prevent further thrombosis (once haemorrhage excluded on CT head)
o Heparin anticoagulation considered if there is a high risk of emboli recurrence or stroke progression
o Formal swallow assessment (NG tube may be needed)
o GCS monitoring
o Thromboprophylaxis
Secondary Prevention
o Aspirin and dipyridamole
o Warfarin anticoagulation (atrial fibrillation)
o Control risk factors: hypertension, hyperlipidaemia, treat carotid artery disease
Surgical Treatment - carotid endarterectomy
Identify the possible complications of stroke (ischaemic and haemorrhagic) and its management
- Cerebral oedema (increased ICP)
- Immobility
- Infections
- DVT
- Cardiovascular events
- Death
Summarise the prognosis for patients with stroke (ischaemic and haemorrhagic)
- 10% mortality in the first month
- Up to 50% that survive will be dependent on others
- 10% recurrence within 1 year
- Prognosis for haemorrhagic is WORSE than ischaemic
Define subarachnoid haemorrhage
• Arterial haemorrhage into the subarachnoid space
Explain the aetiology / risk factors of subarachnoid haemorrhage
- 85% - rupture of a saccular aneurysm at the base of the brain (Berry aneurysms)
- 10% - perimesencephalic haemorrhage
- 5% - arteriovenous malformations, bleeding diathesis, vertebral artery dissection
Risk Factors o Hypertension o Smoking o Excess alcohol intake o Saccular aneurysms are associated with: • Polycystic kidney disease • Marfan's syndrome • Ehlers-Danlos syndrome
Summarise the epidemiology of subarachnoid haemorrhage
- Incidence: 10/100,000
* Peak incidence: 40s
Recognise the presenting symptoms of subarachnoid haemorrhage
- Sudden-onset worst headache ever
- Nausea/vomiting
- Neck stiffness
- Photophobia
- Reduced level of consciousness
Recognise the signs of subarachnoid haemorrhage on physical examination
Meningism
o Neck stiffness
o Kernig’s sign
o Pyrexia
- GCS - check for deterioration
- Signs of raised ICP - papilloedema, IV or III nerve palsies, hypertension, bradycardia
- Focal neurological signs (e.g. cranial nerve palsies)
Identify appropriate investigations for subarachnoid haemorrhage and interpret the results
Bloods o FBC o U&Es o ESR/CRP o Clotting
CT Scan
o Hyperdense areas in the basal regions of the skull (due to blood)
Angiography - detect source of bleeding
Lumbar Puncture
o Increased opening pressure
o Increased red cells
o Xanthochromia - straw-coloured CSF due to breakdown of red blood cells
Define subdural haemorrhage
• A collection of blood that develops between the surface of the brain and the dura mater • Classification o ACUTE: < 72 hrs o SUBACUTE: 3- 20 days o CHRONIC: > 3 weeks
Explain the aetiology / risk factors of subdural haemorrhage
• Trauma (usually due to rapid acceleration and deceleration of the brain)
Summarise the epidemiology of subdural haemorrhage
- Acute - younger patients/associated with major trauma
- MORE COMMON than extradural haemorrhage
- Chronic - more common in the ELDERLY
Recognise the presenting symptoms of subdural haemorrhage
Acute
o History of TRAUMA with head injury
o Reduced conscious level
Subacute
o Worsening headache 7-14 days after injury
o Altered mental state
Chronic o Headache o Confusion o Cognitive impairment o Psychiatric symptoms o Gait deterioration o Focal weakness o Seizures
Recognise the signs of subdural haemorrhage on physical examination
Acute
o Reduced GCS
o Ipsilateral fixed dilated pupil (if a large haematoma cause a midline shift)
o Pressure on brainstem –> reduced consciousness + bradycardia
Chronic
o Neurological examination may be NORMAL
o Focal neurological signs (e.g. 3rd nerve palsy)
Identify appropriate investigations for subdural haemorrhage and interpret the results
- CT Head
* MRI Brain - higher sensitivity than CT
Generate a management plan for subdural haemorrhage
ACUTE
o ALS protocol
o Watch out for cervical spine injury
o If raised ICP consider osmotic diuresis
Conservative - if small
Surgical
o Prompt Burr hole or craniotomy
Chronic
o If symptomatic - Burr hole or craniotomy and drainage
Children
o Younger children may be treated with percutaneous aspiration via an open fontanelle
Identify the possible complications of subdural haemorrhage and its management
- Raised ICP
- Cerebral oedema
- Herniation
- Post-Op - seizures, recurrence, intracerebral haemorrhage, brain abscess, meningitis, tension pneumocephalus
Summarise the prognosis for patients with subdural haemorrhage
Acute
o Underlying brain injury will affect function
Chronic
o Better outcome than subdural haemorrhages
o Lower incidence of underlying brain injury
Define urinary catheterisation
In urinary catheterization a latex, polyurethane, or silicone tube known as a urinary catheter is inserted into a patient’s bladder via the urethra. Catheterization allows the patient’s urine to drain freely from the bladder for collection
Summarise the indications for urinary catheterisation
Specific reasons a urinary catheter may be used include:
to allow urine to drain if you have an obstruction in the tube that carries urine out of the bladder (urethra) – for example, because of scarring or prostate enlargement
to allow you to urinate if you have bladder weakness or nerve damage that affects your ability to pee
to drain your bladder during childbirth if you have an epidural anaesthetic
to drain your bladder before, during or after some types of surgery
to deliver medication directly into the bladder, such as during chemotherapy for bladder cancer
as a last resort treatment for urinary incontinence when other types of treatment have been unsuccessful
Identify the possible complications of urinary catheterisation
The main problems caused by urinary catheters are infections in the urethra, bladder or, less commonly, the kidneys. These types of infection are known as urinary tract infections (UTIs) and usually need to be treated with antibiotics.
You can get a UTI from either short- or long-term catheter use. However, the longer a catheter is used, the greater the risk of infection. This is why it’s important that catheters are inserted correctly, maintained properly, and only used for as long as necessary.
Catheters can also sometimes lead to other problems, such as bladder spasms (similar to stomach cramps), leakages, blockages, and damage to the urethra.
