Acute Care and Trauma Flashcards
What is acute kidney injury (AKI)?
An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output
What is the aetiology of acute kidney injury (AKI)?
AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease
What are the risk factors of acute kidney injury (AKI)?
Advanced age
Underlying kidney disease
Diabetes Mellitus
Sepsis- may result in acute tubular necrosis, infectious glomerulonephritis, pre-kidney AKI from hypotension, or drug-induced injury from medications
Nephrotoxins e.g. aminoglycosides, NSAIDs, vancomycin
What are the pre-renal causes of an AKI?
Reduced renal perfusion:
Shock (hypovolaemic, septic, cardiogenic)
hepatorenal syndrome (liver failure)
What are the renal causes of an AKI?
Acute tubular necrosis- ischaemia, drugs and toxins
Acute glomerulonephritis
Acute interstitial nephritis- NSAIDs, penicillins, sulphonamides
Vessel obstruction- Renal artery/vein thrombosis, cholesterol emboli, vasculitis
Other causes:
myeloma, haemolysis, nephropathy
What are the post renal causes of an AKI?
Stone
Tumour (pelvic, prostate, bladder)
Blood clots
Retroperitoneal fibrosis
What is the epidemiology of AKI?
Incidence of 1800 per million
What are the presenting symptoms of AKI?
Usually asymptomatic Lower urinary tract symptoms- urgency, frequency or hesitancy Low urine output (oliguria) Malaise Anorexia Nausea and vomiting Pruritus (itching) Drowsiness Convulsions, coma (caused by uraemia)
What are the signs of acute kidney injury (AKI) on physical examination?
Oedema
What are the appropriate investigations for AKI and interpret the results?
1st line:
Basic metabolic profile- an acutely rising creatinine may be the only sign. Acutely elevated serum creatinine, high serum potassium, metabolic acidosis.
Serum potassium- elevated in hyperkalaemia
LFTs will be deranged in hepatorenal syndrome
FBC- leukocytosis may suggest an infection
CRP- elevated in infection and vasculitis
Blood culture- Positive for bacterial pathogen
Urinalysis- RBCs, WBCs, cellular casts (glomerulonephritis), proteinuria, positive nitrite, and leukocyte esterase
CXR- signs of infection or fluid
ECG- changes associated with hyperkalaemia (tented T waves)
Others:
Renal ultrasound- check for an obstructive cause
What is the management plan for acute kidney injury?
1.Assess hydration and fluid balance:
Pulse rate, lying and standing BP, JVP, skin turgor, chest auscultation, peripheral oedema, central venous pressure, fluid and weight charts. ECG monitoring (hyperkalaemia)
- If hypovolaemic (+ hyperkalaemia)
- fluid resuscitation
- review medications and stop nephrotoxins
- identify and treat underlying cause
others:
-vasoactive drug
-blood transfusion - If hypervolaemic (+ pulmonary oedema and hyperkalaemia)
- loop diuretic (under specialist supervision) and sodium restriction
- identify and treat underlying cause
consider: renal replacement therapy
Metabolic acidosis (if pH < 7.2): 50–100 mL of 8.4% bicarbonate via central line over 15–30 min
What medications can cause an AKI?
Acute tubular necrosis (ATN): paracetamol, aminoglycosides, amphotericin B (anti-fungal), NSAIDs, ACE-inhibtors, lithium
Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides
Others: opioids, other antibiotics e.g. trimethoprim, vancomycin
What is the treatment for acute pulmonary oedema?
P- positioning (sit up)
O- oxygen
D- diuretic (furosemide) and fluid restriction
M- (dia)morphine
A- anti-emetics
N- nitrates (GTN infusion if SBP >110, or 2 puffs GTN spray if SBP >90)
What are the possible complications of acute kidney injury (AKI)?
Common and life-threatening: Hyperkalaemia Sepsis Metabolic acidosis Pulmonary oedema Hypertension. Less common: Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis
What is the prognosis for patients with acute kidney injury (AKI)?
Acute tubular necrosis has biphasic recovery starting with oliguria then leading to polyuria (resulting from regeneration of the tubular cells).
Prognosis depends on the number of other organs involved, e.g. heart, lung.
Many of those with ATN recover.
Acute cortical necrosis may cause hypertension and chronic renal failure.
What is acute respiratory distress syndrome?
A syndrome of acute and persistent lung inflammation with increased vascular permeability
What are the causes of acute respiratory distress syndrome?
(TOAST) Transfusion Overdose of drugs Aspiration Sepsis Transplantation (PIP) Pneumonia Injury/burns Pancreatitis
What is ARDS characterised by?
A - Absence of raised capillary wedge pressure
R - Reduced blood oxygen (hypoxaemia)
D - Double-sided infiltrates (bilateral infiltrates)
S - sudden onset (acute- within 1 week)
What is the aetiology of acute respiratory distress syndrome?
Severe insult to lungs
Inflammatory mediators released
Capillary permeability increases
Results in pulmonary oedema, reduced gas exchange and reduced lung compliance
(Injury, inflammation, increased permeability)
What is the epidemiology of acute respiratory distress syndrome?
Annual UK incidence 1 in 6000
What are the pathological stages of ARDS?
Exudative
Proliferative
Fibrotic
What are the presenting symptoms of ARDS?
Rapid deterioration of respiratory function
Dyspnoea
Cough
Symptoms of cause
What are the signs of ARDS on physical examination?
Think SMURF: fast, blue, noisy: Cyanosis Tachypnoea Tachycardia Widespread crepitations Hypoxia refractory to oxygen treatment (Usually bilateral but may be asymmetrical in early stages)
What are the appropriate investigations for ARDS? Interpret the results
1st line:
CXR- bilateral infiltrates
ABG- low partial oxygen pressure
Sputum/ blood/ urine cultures- positive if underlying infection
Amylase- elevated in cases of acute pancreatitis
Others:
BNP- <100 nanograms/L make HF less likely, so ARDS more likely
Pulmonary artery catheterisation- Pulmonary artery occlusion pressure (PAOP) ≤18 mmHg suggests ARDS
What is adrenal insufficiency?
Deficiency of adrenal cortical hormones (mineralocorticoids, glucocorticoids and androgens)
What is the aetiology / risk factors of adrenal insufficiency?
Primary (Addisons disease): Autoimmune (>70%)
Secondary: Pituitary or hypothalamic disease.
Surgical: After bilateral adrenalectomy.
Medical: (iatrogenic) sudden cessation of long-term steroid therapy
4Is:
- Infections: Tuberculosis, meningococcal septicaemia (Waterhouse–Friderichsen syndrome), Cytomegalovirus (HIV patients)
- Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis
- Infarction: Secondary to thrombophilia
- Inherited: Adrenoleukodystrophy 1, ACTH receptor mutation
What is the epidemiology of adrenal insufficiency?
Most common cause is iatrogenic. Primary causes are rare
What are the presenting symptoms of adrenal insufficiency?
Chronic presentation:
Non-specific vague symptoms such as dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain, lethargy, weakness, depression
Acute presentation: (Addisonian crisis)
Acute adrenal insufficiency with major haemody-
namic collapse often precipitated by stress (e.g. infection or surgery)
What are the signs of adrenal insufficiency on physical examination?
Postural hypotension
Increased pigmentation: Generalised but more noticeable on buccal mucosa, scars, skin creases, nails, pressure points (resulting from melanocytes being stimulated by increased ACTH levels)
Loss of body hair in women (androgen deficiency)
Associated autoimmune conditions: e.g. vitiligo
Addisonian crisis: Hypotensive shock, tachycardia, pale, cold, clammy, oliguria
What are the appropriate investigations for adrenal insufficiency? Interpret the results
Confirm the diagnosis:
9a. m. serum cortisol <100nmol/L is diagnostic of adrenal insufficiency.
- If 9 a.m. cortisol > 550 nmol/L: adrenal insufficiency is unlikely.
- Patients with 9 a.m. cortisol of between 100 and 550 nmol/L should have a short ACTH stimulation test (short SynACTHen test)
- Serum cortisol <550 nmol/L at 30 min indicates adrenal failure (primary)
Addisonian crisis:
Bloods- Haematology (FBC for neutrophilic, ESR for infection), Biochemistry (U&Es for raised urea and potassium, low sodium, CRP for infection), Microbiology (blood cultures)
Urine- MCS
What is the management for addisonian crisis?
- Rapid IV fluid rehydration (0.9% saline, 1 L over 30–60 min, 2–4 L in 12–24 h)
- 50ml of 50 % dextrose to correct hypoglycaemia.
- IV 200 mg hydrocortisone bolus followed by 100 mg 6 hourly (until BP is stable).
- Treat the precipitating cause (e.g. antibiotics for infection)
- Monitor temperature, pulse, respiratory rate, BP, sat O2 and urine output.
What is the management plan for adrenal insufficiency?
Chronic:
Replacement of glucocorticoids with hydrocortisone (three times/day) and mineralocorticoids with fludrocortisone
Hydrocortisone dosage needs to be increased during acute illness or stress
If associated with hypothyroidism, give hydrocortisone before thyroxine (to avoid precipitating an Addisonian crisis)
Advice: Steroid warning card, Medic-alert bracelet, emergency hydrocortisone ampoule, patient education
What are the possible complications of adrenal insufficiency?
Hyperkalaemia
Death during an Addisonian crisis
What is the prognosis for patients with adrenal insufficiency?
Adrenal function rarely recovers, but normal life expectancy can be expected if treated
What is alcohol withdrawal?
A patient who is alcohol dependent and has stopped or reduced their alcohol intake within hours or days of presentation
What does alcohol dependence mean?
Characterized by three or more of:
. Withdrawal on cessation of alcohol
. Tolerance
. Compulsion to drink, difficulty controlling termination or the levels of use
. Persistent desire to cut down or control use
. Time is spent obtaining, using, or recovering from alcohol
. Neglect of other interests (social, occupational, or recreational)
. Continued use despite physical and psychological problems
What are the risk factors of alcohol withdrawal?
History of alcohol withdrawal syndrome
Abrupt withdrawal of alcohol
What is the aetiology of alcohol withdrawal?
- Alcohol enhances inhibitory GABA activity and inhibits excitatory glutamate neurotransmission.
- Chronic alcohol exposure results in a compensatory reduction in GABA receptor function and upregulation of the glutamate NMDA receptors.
- Abrupt alcohol cessation leads to overactivation of the excitatory NMDA system relative to the GABA system
What is the epidemiology of alcohol withdrawal?
WHO estimates that 43% of the world population consumes alcohol, with 18.2% of drinkers aged over 15 years engaging in heavy episodic alcohol consumption
Up to 25% of people in alcohol withdrawal experience hallucinations, while seizures occur in 10% of patients.
If alcohol withdrawal is not treated or is inadequately treated, 5% of patients will progress to delirium tremens, typically 48 to 72 hours after the last drink
What is delirium tremens?
An acute confusional state caused by the withdrawal of alcohol (48–72h after cessation) Features include: -Sweating -Hallucinations/ delusions/ confusion -Coarse tremor - Agitation - Fever -Tachycardia
What are the presenting symptoms of alcohol withdrawal?
HAD A PINT
Headache
Anxiety/ agitation
Depression
Anorexia
Palpitations
Insomnia
Nausea
Tremor
others: visual hallucinations, confusion, seizures
What are the signs of alcohol withdrawal?
Signs suggestive of chronic alcohol misuse: Dupuytrens contracture Palmar erythema Bruising Spider naevi Telangiectasia- widened venules cause threadlike red lines or patterns on the skin Bilateral parotid enlargement Gynaecomastia Smell of alcohol
What are the appropriate investigations for alcohol withdrawal? Interpret the results
1st line:
VBG- respiratory alkalosis with delirium tremens
Bloods:
- FBC for thrombocytopenia, increased MCV
-Blood glucose for hypoglycaemia
-U&Es for electrolytes deficiencies e.g. hypomagnesaemia, hypokalaemia, hypophosphataemia
-LFTs for elevated liver enzymes (AST, ALT, and GGT)
- bone profile for hypocalcaemia
- coagulation studies for chronic liver disease (prolonged INR and prothrombin time)
Others:
Toxic screen- barbiturates, paracetamol
What is the management plan for a patient with alcohol withdrawal?
*ABCDE* Amobarbital (hypnotic and anxiolytic) (IV) B1 vitamin (thiamine) Chloro- Diaz- Epoxide
*chlorodiazepoxide is a benzodiazepine
What are the possible complications of alcohol withdrawal?
Seizures, delirium tremens Chronic complications include: Cerebral atrophy and dementia Cerebellar degeneration Optic atrophy Peripheral neuropathy Myopathy.
Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernickes encephalopathy or Korsakoffs psychosis
What is the prognosis for patients with alcohol withdrawal?
Depends on complications.
Alcoholic fatty liver is reversible on abstinence from alcohol. In general, 5-year survival rates in those with alcoholic cirrhosis who stop drinking are 60–75%, but < 40% in those who continue
What is the reason for fatality in alcohol withdrawal?
Seizures (generalised tonic-clonic)
What is anaphylaxis?
Acute life-threatening multisystem hypersensivity syndrome caused by sudden release of mast cell- and basophil-derived mediators into the circulation
What is anaphylaxis characterised by?
Rapidly developing life-threatening airway and/or breathing and/or circulation problems
Usually associated with skin and mucosal changes
What is the aetiology of anaphylaxis?
Immunologic: IgE-mediated or immune complex/complement-mediated
Non-immunologic: mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Inflammatory mediators such as histamine cause bronchospasm, increased capillary permeability and
reduced vascular tone, resulting in tissue oedema
What are the common allergens?
PILFERS
Peanuts Insect stings Latex Fish Egg Radiological contrast agents Shellfish
What is the epidemiology of anaphylaxis?
Relatively common
What are the presenting symptoms of anaphylaxis?
Acute onset of symptoms on exposure to allergen (SOB):
Skin (rash, pruritis)
Oedema (lips, face)
Breathing (short of breath, wheezing)
Biphasic reactions occur 1–72 h after the first reaction in up to 20% of patients
What are the signs of anaphylaxis on physical examination?
URTICARIA: Urticaria Reduced BP Tachypnoea Infected conjunctiva and swollen eyes Cyanosis Audible wheeze Rhinitis Increased heart rate Airway swelling
What are the appropriate investigations for anaphylaxis? Interpret the results
The diagnosis of anaphylaxis is made clinically.
1st line:
Serum (mast cell) tryptase (measured within 15 min–3 h after onset of symptoms)= elevated
Histamine levels (measured preferably within 30 min after symptom onset)
Urinary metabolites of histamine (which may remain elevated for several hours after symptom onset)
ABG: elevated lactate
ECG: Non-specific ST ECG changes are common post-adrenaline
What is the management plan for a patient with anaphylaxis?
Oxygen Can Help Anaphylaxis: Oxygen (100%) Chloropheniramine (10mg) Hydrocortisone (100mg) Adrenaline (IM)- 0.5 mL of 1:1,000, can be repeated every 10mins according to response of pulse and BP
Advice: Educate on use of adrenaline pen for IM administration. Provide Medicalert bracelet
What are the possible complications of anaphylaxis?
(RDS)
Respiratory failure
Death
Shock
What is the prognosis for patients with anaphylaxis?
Good if prompt treatment given
What is an arterial blood gas (ABG)?
A procedure to measure the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery
What are the indications for an arterial blood gas?
Respiratory failure - in acute and chronic states.
Any severe illness which may lead to a metabolic acidosis:
Cardiac failure
Liver failure
Renal failure
Hyperglycaemic states associated with diabetes mellitus
Multiorgan failure
Sepsis
Burns
Poisons/toxins
PLUS Ventilated patients
What are the possible complications of an arterial blood gas?
Local hematoma Arterial vasospasm Arterial occlusion Air or thrombus embolism Local anesthetic anaphylactic reaction Infection at the puncture site
What is aspirin overdose?
Excessive ingestion of aspirin (salicylates) causing toxicity
What are the risk factors of aspirin overdose?
Overdose can occur as a result of: Deliberate self-harm Suicidal intent By accident (e.g. in children) Ingestion of 10–20 g can cause moderate-to-severe toxicity in adults.
What is the aetiology of aspirin overdose?
- Aspirin (acetylsalicylate) increases respiratory rate and depth by stimulating the CNS respiratory centre.
- This hyperventilation produces respiratory alkalosis in the early phase.
- The body then compensates by increasing urinary bicarbonate and K+ excretion, causing dehydration and hypokalaemia.
- Loss of bicarbonate together with the uncoupling of mitochondrial oxidative phosphorylation by salicylic acid and build up of lactic acid can lead to metabolic acidosis.
What is the epidemiology of aspirin overdose?
One of the most common drug overdoses
What are the presenting symptoms of aspirin overdose?
The patient may be asymptomatic initially.
Early symptoms: Flushed appearance, fever, sweating, hyperventilation, dizziness, tinnitus, deafness.
Late symptoms: Lethargy, confusion, convulsions, drowsiness, respiratory depression, coma
OVERDOSE Over- Ventillation Ears ringing (tinnitus) Red-faced (flushed appearance) Dizziness Overtired Sweating (fever) Epileptic-looking (convulsions)
What are the signs of aspirin overdose on physical examination?
Fever
Tachycardia
Hyperventillation
Epigastric tenderness
What are the appropriate investigations for aspirin overdose. Interpret the results
ABG: initially respiratory alkalosis; later concomitant metabolic acidosis
Salicylate levels: (500–750mg/L is a moderate overdose; >750mg/L is a severe overdose)
Bloods:
-Serum electrolytes: hypokalaemia, hypocalcaemia, and/or hypomagnesaemia
-FBC: WBC may be elevated
-LFTs: AST and ALT may be elevated
ECG: May show signs of hypokalaemia – small T waves, U waves
What is asthma?
Chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
What are the risk factors of asthma?
Genetic factors:
Family Hx
Atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens)- eczema, atopic dermatitis, allergic rhinitis is strongly associated
Environmental factors: House dust mite Pollen, Pets (e.g. urinary proteins, furs) Cigarette smoke Viral respiratory tract infection Aspergillus fumigatus spores
What is the pathogenesis of asthma?
Early phase (up to 1 h): Exposure to inhaled allergens results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
Late phase (after 6–12h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
Airway remodelling: the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts from cytokines and proliferative growth factors
What is the epidemiology of asthma?
Affects 10% of children and 5% of adults
Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK
What are the presenting symptoms of asthma?
Episodes of wheeze Breathlessness Cough Worse in the morning and at night Interfering with exercise, sleeping, school/ work
What are the exacerbating factors of asthma?
Cold Viral infections Drugs (b-blockers, NSAIDs) Exercise Emotions
What are the signs of asthma on physical examination?
Tachypnoea Use of accessory muscles Prolonged expiratory phase Polyphonic wheeze* on expiration Hyper inflated chest
What are the signs of a severe asthma attack?
PEFR < 50% predicted
HR > 110/min (tachycardia)
RR > 25/min
Inability to complete sentences
What are the signs of a life threatening asthma attack?
PEFR<33% Silent chest Bradycardia Hypotension Confusion Coma Cyanosis
What are the appropriate investigations for asthma? Interpret the results
1st line:
- FEV1/FVC: <70% of predicted
- Peak flow
- CXR: hyper inflated lungs
- FBC: Eosinophilia
What is the acute management of asthma?
O SHIT ME
Oxygen (high flow)
Salbutamol- 2.5-5mg NEB
Hydrocortisone- 100mg IV (or prednisolone 40mg PO)
Ipratropium- 500mcg NEB
Theophylline*: aminophylline infusion- 1g in 1L saline 0.5ml/kg/h
Magnesium sulphate- 2g IV over 20mins Escalate care (intubation and ventilation)
*smooth muscle relaxation (bronchodilation) and suppression of the response of the airways to stimuli
What is the chronic management for asthma? (Stepwise)
Step 1: Inhaled short acting B2 agonist as needed (if used >1 / day move to 2)
Step 2: Step 1 + regular inhaled lose dose steroids (400mcg/day)
Step 3: Step 2 + long acting B2 agonist (if inadequate control increase steroid dose to 800mcg/day)
Step 4: Step 3 + increase inhaled steroid dose to 2000mcg/day and add 4th drug (leukotriene receptor antagonist or B2 agonist tablet)
Step 5: Step 4 + addition of regular oral steroids (maintain high dose inhaled steroids) and refer to specialist
review every 3-6 months
1: SABA
2: SABA + inhaled steroid
3: SABA + inhaled steroid (high dose if needed) + LABA
4: SABA + LABA + high dose inhaled steroids + leukotriene receptor antagonist
5: SABA + LABA + high dose inhaled steroids + leukotriene receptor antagonist + regular oral steroids and refer to specialist
What are the complications of asthma?
Growth retardation
Pectus carinatum (pigeon chest)
Recurrent infections
Pneumothorax
What is the prognosis for patients with asthma?
Children: many improve as they grow
Adults: adult onset is usually chronic
What is a burns injury?
A very common injury predominantly to skin and superficial tissues caused by heat from hot liquids, flame or contact with hot objects
How is the severity of burns injuries assessed?
- Burn size (% of total body surface area)
- Depth ( first to fourth degree)
What symptoms and signs would be seen on physical examination for burns injuries?
Erythema Dry/ wet and painful Dry and lacking of physical sensation (insensate) Cellulitis If face affected- clouded cornea
What are the risk factors for burn injuries?
Young children
Age > 60 years
What are the investigations for burn injuries?
FBC: Hb, Platelets, WCC, CRP, ESR
ABG: assessment of lungs/ inhalation injury
Wound biopsy and histology
What is the management for a burns injury?
Initial treatment: wound cooling, cleaning and dressing
Then: topical antibiotic prophylaxis, tetanus immunisation and opioid analgesia
What is the prognosis for a burns injury?
*depends on the severity of the burn
Associated injuries e.g. inhalation injury/ trauma adversely affect the prognosis
What are the three severities of burns injuries and the approximate healing time for each of them?
- Superficial - 7 days
- Deep - 21 days
- Full thickness - requires skin graft
What is cardiac arrest?
Acute cessation of cardiac function
What are the reversible causes for a cardiac arrest?
4 Hs and 4Ts: Hypokalaemia Hypothermia Hypovolaemia Hypoxia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins
What signs would be seen on physical examination for a a patient in cardiac arrest?
Unconscious
Patient is not breathing
Absent carotid pulses
What are the 4 cardiac rhythm disturbances?
Ventricular fibrillation (VF)
Pulseless ventricular tachycardia (VT)
Pulseless electrical activity
Asystole
What are the appropriate investigations for a cardiac arrest?
Cardiac monitor: Classification of the rhythm directs management
Bloods: ABG, U&Es, FBC, cross-match, clotting, toxicology screen, glucose.
What is the management for a cardiac arrest?
Safety: approach with caution, defibrillators and oxygen are hazards- call for help
A: Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift.
B: Assess breathing by look, listen and feel.
If not breathing, give two effective breaths immediately.
C: Assess circulation at carotid pulse for 10 s.
If absent, give 30 chest compressions at rate of 100/min. Continue cycles of 30 compressions for every two breaths.
Proceed to advanced life support as soon as possible.
What is the advanced life support for a cardiac arrest?
- Attach cardiac monitor and defibrillator
2. Assess the rhythm
What cardiac rhythms are shockable?
Ventricular tachycardia
Ventricular fibrillation
What is the management for shockable cardiac rhythms?
- Defibrillate once
- Resume CPR immediately for 2 min, and then defibrillate
- Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
- If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(anti-arrhythmic)
What cardiac rhythms are non-shockable?
Pulseless electrical activity
Asystole
What drug is given in asystole or PEA cardiac arrests?
Atropine (3 mg IV, once only) if asystole or PEA with rate <60/min
What is the management for non- shockable cardiac rhythms?
- CPR for 2 min, and then return to assessing rhythm
- Administer adrenaline (1 mg IV) every 3–5 min.
- Atropine (3 mg IV, once only) if asystole or PEA with rate <60/min
What is the treatment for the reversible causes of cardiac arrest?
Hypothermia: Warm slowly
Hypo- or hyperkalaemia: Correction of electrolytes
Hypovolaemia: IV colloids, crystalloids or blood products
Hypoxia: oxygen
Tamponade: Pericardiocentesis under xiphisternum up and leftwards
Tension pneumothorax: Needle into second intercostal space, mid-clavicular line
Thromboembolism: management for PE, MI
Toxins: antidotes
What are the complications of a cardiac arrest?
Irreversible hypoxic brain damage, death
What is the prognosis for patients with a cardiac arrest?
Resuscitation is less successful in the arrests that occur outside hospital.
Duration of inadequate effective cardiac output is associated with poor prognosis.
What is Blood product transfusion?
A lifesaving procedure to treat hemorrhages and to improve oxygen delivery to tissues
What are the indications for Blood product transfusion (red cell)?
Symptomatic anemia (causing shortness of breath, dizziness, congestive heart failure, and decreased exercise tolerance)
Acute sickle cell crisis
Acute blood loss of more than 30 percent of blood volume
What are the indications for Blood product transfusion (fresh frozen plasma)?
Can be used for reversal of anticoagulant effects
What are the indications for Blood product transfusion (Platelet transfusion)?
To prevent haemorrhage in patients with thrombocytopenia or platelet function defects
What are the indications for Blood product transfusion (Cryoprecipitate)?
Used in cases of hypofibrinogenemia, which most often occurs in the setting of massive hemorrhage or consumptive coagulopathy
What are the possible complications of Blood product transfusion?
Acute complications occur within minutes to 24 hours of the transfusion, whereas delayed complications may develop days, months, or even years later
*Infections are less common because of advances in the blood screening process
Non-infectious complications (acute): -Acute haemolytic reaction -Allergic/Anaphylactic reaction -Coagulation problems in massive transfusion -Metabolic derangements -Septic or bacterial contamination -Transfusion-associated circulatory overload Non-infectious complications (delayed): -Delayed haemolytic reaction -Iron overload -Post-transfusion purpura
Infectious complications:
- Hepatitis B virus
- Hepatitis C virus
- Human T-lymphotropic virus 1 or 2
- Human immunodeficiency virus
What is cardiac failure?
Inability of the cardiac output to meet the bodys demands despite normal venous pressures
What is the aetiology of low output cardiac failure?
Left heart failure: -Ischaemic heart disease -Hypertension -Cardiomyopathy -Aortic valve disease -Mitral regurgitation Right heart failure: -Secondary to left heart failure -Infarction -Cardiomyopathy -Pulmonary hypertension/embolus/valve disease -Chronic lung disease -Tricuspid regurgitation -Constrictive pericarditis/pericardial tamponade Biventricular failure: -Arrhythmia -Cardiomyopathy (dilated or restrictive) -Myocarditis -Drug toxicity
What is the aetiology of high output cardiac failure?
(High demand) Anaemia Beriberi (vitamin B-1 deficiency- thiamine deficiency) Pregnancy Pagets disease Hyperthyroidism Arteriovenous malformation
What is the epidemiology of cardiac failure?
10% of > 65-year-olds
What are the presenting symptoms of left sided cardiac failure?
Left (symptoms caused by pulmonary congestion): Dyspnoea (New York Heart Association classification): 1. no dyspnoea 2. dyspnoea on ordinary activities 3. dyspnoea on less than ordinary activities 4. dyspnoea at rest Orthopnoea Paroxysmal nocturnal dyspnoea Fatigue
What are the presenting symptoms of right sided cardiac failure?
Swollen ankles Fatigue Increased weight (resulting from oedema) Reduced exercise tolerance Anorexia Nausea
What are the signs of left sided cardiac failure on physical examination?
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
Third heart sound (gallop rhythm: rapid ventricular filling)
Pansystolic murmur (functional mitral regurgitation)
What are the symptoms and signs of ACUTE left ventricular cardiac failure?
Symptoms: Dyspnoea, wheeze, cough and pink frothy sputum
Signs: Tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans (strong and weak beats), gallop rhythm, wheeze cardiac asthma, fine crackles throughout the lung
What are the signs of right sided cardiac failure on physical examination?
Raised JVP Hepatomegaly Ascites Ankle/sacral pitting oedema Signs of functional tricuspid regurgitation
What are the appropriate investigations for cardiac failure?
Bloods:
- Elevated BNP (B type natriuretic peptide, associated with reduced LVEF)
- FBC (anaemia, high lymphocytes)
- U&Es baseline (decreased sodium, altered potassium)
- Serum creatinine: normal to elevated
- LFTs: normal to elevated (reflects abdominal congestion)
- TFTs: screening for hypo and hyperthyroidism
- Others: CRP, glucose, lipids
CXR:
- Cardiomegaly (heart >50 % of thoracic width)
- Pulmonary vascular congestion (vascular redistribution, Kerley B lines-interstitial oedema)
- Pleural effusion (usually right-sided but often bilateral)
ECG: May be normal. May show underlying coronary artery disease, left ventricular hypertrophy, or atrial enlargement
Echocardiogram: To assess ventricular contraction
- If left ventricular ejection fraction (LVEF) <40%: systolic dysfunction
- Diastolic dysfunction: reduced compliance leading to a restrictive filling defect
Swan–Ganz catheter (right heart catheterisation):
Allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures (any pulmonary or systemic resistance)
Exercise stress testing/exercise tolerance:
Assess patient’s functional exercise limitation and haemodynamic response to exercise
What are the appropriate investigations for acute cardiac failure?
Bloods:
-FBC (anaemia)
-ABG
-Troponin: elevated
-Brain natriuretic peptide (BNP): elevated suggests the
diagnosis of cardiac failure
*A low plasma BNP rules out cardiac failure (90% sensitivity)
ECG: arrhythmia (20% are AF) , ischaemic ST and T wave changes
CXR:
- Cardiomegaly
- Pulmonary congestion
- Pleural effusion
- Valvular or pericardial calcification
Echocardiogram:
-Abnormal systolic and diastolic function (EF)
Cardiac catheterisation: abnormal coronary artery flow and left ventricular function
What is the management for acute cardiac failure?
Cardiogenic shock:
Severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine) and should be managed in ITU
*inotropes: increase the force contractility of the heart
Pulmonary oedema:
Sit up patient, 60–100% O2 and consider CPAP. Other first-line therapies are diamorphine (venodilator and anxiolytic effect), GTN infusion (reduces preload), IV furosemide if fluid overloaded (venodilator and later diuretic effect)
Monitor BP, respiratory rate, sat. O2, urine output, ECG. Treat the cause, e.g. myocardial infarction, arrhythmia
What is the management for chronic cardiac failure?
Treat the cause, e.g. hypertension
Treat exacerbating factors, e.g. anaemia
- ACE-inhibitors (e.g. enalapril, perindopril, ramipril):
Inhibit intracardiac renin-angiotensin system which may contribute to myocardial hypertrophy and remodelling. ACE inhibitors slow progression of the heart failure and improve survival - b-Blockers (bisprolol or carvedilol): Block the effects of chronically activated sympathetic system, slow progression of the heart failure and improve survival. The benefits of ACE inhibitors and b-blockers are additive*
- Loop diuretics (e.g. furosemide) and dietary salt restriction to correct fluid overload.
- Aldosterone antagonists (spironolactone or, if not tolerated, eplerenone) improve survival. May be used to assist in the management of diuretic-induced hypokalaemia
- Angiotensin receptor blockers (ARB) (e.g. candesartan): May be added in patients with persistent symptoms despite ACE inhibitors and b-blockers.
- Hydralazine and a nitrate: May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker
- Digoxin: Positive inotrope, reduces hospitalization, but does not improve survival
- Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and survival in patients with LVEF 35%.
Most patients who meet these criteria are also candidates for an implantable cardiac defibrillator (ICD) and receive a combined device
*Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil)
What are the complications of cardiac failure?
Respiratory failure, cardiogenic shock, death
What is the prognosis of cardiac failure?
50% of patients with severe heart failure die within 2 years
What is Chronic obstructive pulmonary disease (COPD)?
A preventable and treatable disease state characterised by airflow limitation that is not fully reversible.
It encompasses both emphysema and chronic bronchitis
What is the aetiology of COPD?
Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke). Overlaps and may co-exist with asthma
What is Chronic bronchitis?
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
What is emphysema?
Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles
What is the aetiology of Chronic bronchitis?
Narrowing of the airways resulting from bronchiole inflammation (bronchiolitis) and bronchi with mucosal oedema, mucous hypersecretion and squamous metaplasia
What is the aetiology of emphysema?
Destruction and enlargement of the alveoli
This results in loss of the elastic traction that keeps small airways open in expiration
Progressively larger spaces develop, termed bullae (diameter is >1 cm)
What is the epidemiology of COPD?
Very common (prevalence up to 8%) Presents in middle age or later (65 years and older) More common in males, but likely to change with increased no. female smokers
What are the presenting symptoms of COPD?
Chronic cough and sputum production Breathlessness Wheeze Reduced exercise tolerance (may present with recurrent lung infections)
What are the signs of COPD on physical examination?
Inspection: -May have respiratory distress -use of accessory muscles -barrel-shaped overinflated chest -decreased cricosternal distance -peripheral/central cyanosis Percussion: -Hyper-resonant chest -loss of liver and cardiac dullness. Auscultation: -Quiet breath sounds -prolonged expiration -wheeze -rhonchi (continuous low pitched, rattling lung sounds- sounds like snoring) -crepitations sometimes present. Signs of CO2 retention: Bounding pulse, warm peripheries, flapping tremor of the hands (asterixis). In late stages, signs of right heart failure (e.g. right ventricular heave, raised JVP, ankle oedema)
What are the appropriate investigations for COPD?
*Spirometry and pulmonary function tests:
Obstructive picture as reflected by reduced PEFR, reduced FEV1: FVC ratio
Pulse oximetry: low oxygen saturation
CXR: May appear normal or show hyperinflation (>6 ribs visible anteriorly, flat hemi- diaphragms), reduced peripheral lung markings, elongated cardiac silhouette
Bloods: FBC ( increasedHb and PCV as a result of secondary polycythemia)
ABG: May show hypoxia (low PaO2), normal or high PaCO2
ECG and echocardiogram: For cor pulmonale
Sputum and blood cultures: In acute exacerbations for treatment
What could be another cause of COPD?
Alpha 1-antitrypsin deficiency (<1%) but should be considered in young patients or in those who have never smoked
What can the FEV1: FVC ratio tell us about the stage of COPD?
Mild 60–80%
Moderate 40–60%
Severe <40%
What is the management for COPD?
Stop smoking.
Bronchodilators: Short-acting b2-agonists (e.g. salbutamol) and anticholinergics (e.g. ipratropium), delivered by inhalers or nebulisers. Long-acting bronchodilators should be used if >2 exacerbations per year
Steroids: Inhaled beclometasone should be considered for all with FEV1 <50% predicted or
those with >2 exacerbations per year.
Regular oral steroids should be avoided but may be necessary for maintenance.
-Chest physiotherapy: for airway clearance
-Pulmonary rehabilitation
-Diet and exercise, patient education (flu vaccination)
-Long-term home oxygen therapy for non-smokers (improves mortality)
What are the complications of COPD?
Acute respiratory failure
Infections (particularly Streptococcus pneumoniae, Haemophilus influenzae)
Pulmonary hypertension and right heart failure
Pneumothorax (resulting from bullae rupture)
Secondary polycythaemia
What is the prognosis for COPD?
Variable prognosis- depends on several factors including genetic predisposition, environmental exposures, co-morbidities and acute exacerbations
High level of morbidity:Three-year survival rate of:
- 90% if age <60 years and FEV1 >50% predicted
-75% if >60 years and FEV1 40–49% predicted
What is Diabetic Ketoacidosis?
An acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment
It is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes mellitus
What is the aetiology of Diabetic Ketoacidosis?
Reduced Insulin and increased counter-regulatory hormones result in increased hepatic gluconeogenesis and reduced peripheral glucose utilization. Renal reabsorptive capacity of glucose is exceeded causing glycosuria, osmotic diuresis and dehydration. Increased lipolysis leads to ketogenesis and metabolic acidosis
The two most common precipitating events are:
- Infection
- Discontinuation of, or inadequate, insulin therapy
Underlying medical conditions, such as myocardial infarction or pancreatitis, that provoke the release of counter-regulatory hormones are also likely to result in DKA in patients with diabetes
What is the epidemiology of Diabetic Ketoacidosis?
The incidence of hospital admissions for DKA among adults with Type 1 AND type 2 diabetes mellitus has increased
What are the presenting symptoms of Diabetic Ketoacidosis?
PMH of DM Nausea and vomiting Abdominal pain Dehydrated Hyperventilation Acetone smell on breath Confusion
What are the signs of Diabetic Ketoacidosis on physical examination?
Signs of dehydration: -Dry mucous membranes -Decreased skin turgor or skin wrinkling -Slow capillary refill -Tachycardia with a weak pulse -Hypotension Polyuria Polydipsia Kussmaul breathing (deep and rapid) Ketotic breath Coma
What are the appropriate investigations for Diabetic Ketoacidosis?
Venous blood gas:
-Metabolic acidosis (pH can determine the severity of DKA)
-pH ≥7.0 indicates mild or moderate DKA
-pH <7.0 indicates severe DKA (critical care)
-Hyperkalaemia is common
-Plasma osmolality is high (>320 mmol/kg) in DKA and is an indication of dehydration
Blood ketones: ketonaemia (ketones ≥3.0 mmol/L)
Blood glucose: hyperglycaemia (blood glucose >11.1 mmol/L)
U&Es: Hyponatraemia and Hyperkalaemia are common in DKA, but hypokalaemia is an indicator of severe
FBC: Leukocytosis is common in DKA and correlates with blood ketone levels
Urinalysis: ketones, leukocytes
ECG: look for cardiac precipitates for DKA such as MI (and check cardiac enzymes)
Pregnancy test
Amylase and lipase: for pancreatitis
Creatinine kinase: elevated with rhabdomyolysis (breakdown of damaged skeletal muscle)
CXR: if low oxygen sats
Blood cultures: if infection suspected
What is the management of Diabetic Ketoacidosis?
URGENT: Start intravenous fluids as soon as DKA is confirmed (fluid bolus of 500 mL of normal saline), repeat if SBP remains low (<90mmHg)
Start a fixed-rate intravenous insulin infusion
Ensure continuous cardiac monitoring
Identify and treat any precipitating acute illness e.g. MI, sepsis, pancreatitis
What are the complications of Diabetic Ketoacidosis?
Cerebral oedema/brain injury most common cause of mortality in DKA
Arterial or venous thromboembolic events: Standard prophylactic low-dose heparin
SE of high insulin dose therapy: hypokalaemia, hypoglycaemia
Pulmonary oedema/ARDS: rare but significant complications of treatment for DKA (fluid overload)
What is the prognosis for Diabetic Ketoacidosis?
Improved understanding of the pathophysiology of DKA, together with close monitoring and correction of electrolytes, has resulted in a significant reduction in the overall mortality rate from this life-threatening condition
Death is rarely caused by the metabolic complications of hyperglycaemia or ketoacidosis but rather relates to the underlying illness
*The prognosis is substantially worsened at the extremes of age and in the presence of coma and hypotension
What is Disseminated intravascular coagulation (DIC)?
An acquired syndrome characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors
Thrombi may lead to vascular obstruction/ischaemia and multi-organ failure
What is the aetiology of Disseminated intravascular coagulation (DIC)?
Disease states that trigger systemic activation of coagulation may lead to DIC. Causes include:
- Sepsis/severe infection, major trauma or burns
- Some malignancies (acute myelocytic leukemia or metastatic mucin-secreting adenocarcinoma)
- Obstetric disorders (amniotic fluid embolism, eclampsia, abruptio placentae, retained dead fetus syndrome)
- Severe organ destruction or failure (severe pancreatitis, acute hepatic failure)
- Vascular disorders (Kasabach-Merritt syndrome or giant haemangiomas, large aortic aneurysms)
- Severe toxic or immunological reactions (blood transfusion reaction or haemolytic reactions, organ transplant rejection, snake bite)
What is the epidemiology of Disseminated intravascular coagulation (DIC)?
Many conditions can cause DIC, therefore, the overall incidence is difficult to determine
Seen in any severely ill patient
What are the presenting symptoms of Disseminated intravascular coagulation (DIC)?
The patient is severely unwell with symptoms of:
- The underlying disease
- Confusion
- Dyspnoea
- Evidence of bleeding
What are the signs of Disseminated intravascular coagulation (DIC) on physical examination?
Signs of the underlying aetiology, fever, evidence of shock (hypotension, tachycardia, oliguria)
Acute DIC:
-Petechiae
-Purpura
-Ecchymoses
-Epistaxis
-Mucosal bleeding
-Overt haemorrhage
-Signs of end organ damage (e.g. local infarction or gangrene), respiratory distress, oliguria caused by renal failure
Chronic DIC:
-Signs of deep venous or arterial thrombosis or embolism
-Superficial venous thrombosis, especially without varicose veins
What are the appropriate investigations for Disseminated intravascular coagulation (DIC)?
Blood:
FBC:
-Decreased platelets (due to excessive consumption)
-Decreased fibrinogen (due to excessive consumption)
-Prolonged prothrombin time
-Elevated D dimer
-Raised fibrin degradation products
Peripheral blood film:
-Red blood cell fragments (schistocytes)
Other investigations according to aetiology
What is Encephalitis?
Inflammation of the brain parenchyma
What is the aetiology for Encephalitis?
In the majority of cases encephalitis is the result of a viral infection. Most common in the UK is HSV.
Other: bacteria (syphilis, staph A), immunocompromised (Cytomegalovirus, toxoplasmosis, Listeria)
What is the epidemiology of Encephalitis?
Annual UK incidence is 7.4 in 100,000
What are the presenting symptoms for Encephalitis?
Usually encephalitis is a mild self-limiting illness.
Subacute onset (hours to days) headache
Fever
Vomiting
Neck stiffness, photophobia, i.e. symptoms of meningism (meningoencephalitis) with behavioural changes
Drowsiness and confusion
There is often a history of seizures
Focal neurological symptoms (e.g. dysphasia and hemiplegia) may be present
It is important to obtain a detailed travel history
What are the signs of Encephalitis on physical examination?
Reduced level of consciousness with deteriorating GCS, seizures, pyrexia.
Signs of meningism: Neck stiffness, photophobia, Kernigs test positive.
Signs of raised intracranial pressure: hypertension, bradycardia, papilloedema.
Focal neurological signs.
Minimental examination may reveal cognitive or psychiatric disturbances.
What is Kernigs sign?
Positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance)- indicating the presence of meningitis or subarachnoid haemorrhage
What are the appropriate investigations for Encephalitis?
Blood: FBC (raised lymphocytes), U&Es (SIADH may occur), glucose (compare with CSF glucose), viral serology, ABG.
MRI/CT: Excludes mass lesion. HSV produces characteristic oedema of the temporal lobe on MRI.
Lumbar puncture: raised Lymphocytes,monocyte and protein, glucose usually normal. Viral PCR is first line.
EEG: May show epileptiform activity, e.g. spiking activity in temporal lobes
What is an epidural?
An anaesthetic injected into the epidural space surrounding the fluid-filled sac (the dura) around the spinal cord. It partially numbs the abdomen and legs and is most commonly used during childbirth.
What are the indications for an epidural?
Provide analgesia:
- intraoperative
- postoperative
- peripartum (labour analgesia, Caesarean section)
- end-of-life settings
Can be used as the primary anaesthetic for surgeries from the mediastinum to the lower extremities
What are the possible complications of an epidural?
Drug related: -anaphylaxis due to allergy due to anaesthetic Procedure related: -back pain -pneumocephalus (presence of air/gas in the cranial cavity) Potentially life-threatening: Subdural injection of LAs Total or high spinal, infectious or aseptic meningitis Cardiac arrest Spinal epidural abscess Epidural hematoma formation Permanent neurologic injury
What is Epilepsy?
A chronic disorder that causes unprovoked, recurrent seizures (Paroxysmal synchronised cortical electrical discharges)
What are the two types of seizures?
Focal seizure:
-Seizure localised to specific cortical regions, such as temporal lobe seizures, frontal lobe seizures, occipital seizures, complex partial seizures
Generalised seizure:
Seizures which affect consciousness typically tonic-clonic, absence attacks, myoclonic, atonic (drop attacks) or tonic seizures
What is the aetiology of Epilepsy?
*The majority of cases are idiopathic
Primary epilepsy syndromes (e.g. idiopathic generalised epilepsy, temporal lobe epilepsy, juvenile myoclonic epilepsy)
Secondary seizures (symptomatic epilepsy):
-Tumour
-Infection (e.g. meningitis, encephalitis, abscess)
-Inflammation (vasculitis, rarely multiple sclerosis)
-Toxic/metabolic (sodium imbalance, hyper- or hypoglycaemia, hypocalcaemia, hypoxia, porphyria, liver failure)
-Drugs (e.g. including withdrawal e.g.alcohol, benzodiazepines)
-Vascular (haemorrhage, infarction)
-Congenital anomalies (e.g. cortical dysplasia)
-Neurodegenerative disease (e.g. Alzheimers disease)
-Malignant hypertension or eclampsia
-Trauma
What are common seizure mimics?
Syncope
Migraine
Non-epileptiform seizure disorder (e.g. dissociative disorder)
What is the epidemiology of Epilepsy?
Common
Prevalence in 1% of general population
Peak age of onset is in early childhood or in the elderly
What is the pathophysiology of Epilepsy?
Seizures result from an imbalance in the inhibitory and excitatory currents (e.g. Na+ or K+ ion channels) or neurotransmission (i.e. glutamate or GABA neurotransmitters) in the brain
What are the presenting symptoms of Epilepsy: Focal seizures?
Frontal lobe focal motor seizues:
Motor convulsions
May demonstrate Jacksonian march (spasm spreading from mouth or digit)
There may be post-ictal flaccid weakness (Todds paralysis)- on one side
Temporal lobe seizures:
Aura (visceral and psychic symptoms: fear or deja-vu sensation)
Hallucinations (olfactory, gustatory)
Frontal lobe complex partial seizures:
Loss of consciousness with associated automatisms and rapid recovery
May be postictal aphasia seen after focal-onset seizures
What are the presenting symptoms of Epilepsy: Generalised seizures?
Tonic-clonic (grand mal):
Vague symptoms before an attack (e.g. irritability), followed by tonic phase (generalised muscle spasm), followed by a clonic phase (repetitive synchro- nous jerks), and associated faecal or urinary incontinence, tongue biting
After a seizure, there is often impaired consciousness, lethargy, confusion, headache, back pain, stiffness
Absence (petit mal):
Usual onset in childhood
Characterized by loss of consciousness but maintained posture (patient stops talking and stares into space for seconds), blinking or rolling up of eyes with other repetitive motor actions (e.g. chewing)
No postictal phase.
Non-convulsive status epilepticus:
Acute confusional state
Often fluctuating
Difficult to distinguish from dementia.
What are the signs of Epilepsy on physical examination?
Depends on aetiology, usually normal between seizures Look for focal abnormalities indicative of brain lesions
What are the appropriate investigations for Epilepsy?
Bloods:
- FBC: if raised WCC, may indicate an infectious cause
- U&Es: electrolyte imbalance can lead to a provoked generalised tonic-clonic seizure
- Glucose: extreme hypoglycaemia or hyperglycaemia can cause provoked generalised tonic-clonic seizures
- Toxicology screen: identify cause
- Prolactin, helps to distinguish a generalised tonic-clonic seizure (GTCS) from a non-epileptic event (transient increase shortly after a true seizure)
- Creatinine Kinase (Elevated in true seizures)
EEG:
- Indicated after any unprovoked seizure event
- Helps confirm or refute the diagnosis; assists in classifying the epileptic syndrome: generalised epileptiform activity or focal, localising abnormality
- Usually performed inter-ictally and often normal and does not rule out epilepsy
CT/MRI:
For structural, space-occupying and vascular lesions
Other investigations: Particularly for secondary seizures according to suspected aetiology e.g. lumbar puncture (infections), HIV serology
What is the management of Epilepsy?
Only start anti-convulsant therapy after >2 unprovoked seizures:
- Lamotrigine: newer agent
- Topiramate: newer agent
- Oxcarbazepine
- Carbamazepine: reasonable choice
- Levetiracetam
- Valproic acid* contraindicated in pregnant women or women of a child bearing age
- Other medications: Phenytoin and Gabapentin
Patient education:
- Avoid triggers (e.g. alcohol)
- Encourage seizure diaries
- Recommend supervision for swimming or climbing, driving is only permitted if seizure free for 6 months
- Women of childbearing age should be counseled regarding possible teratogenic effects of AEDs and should consider taking supplemental folate to limit the risk
- Drug interactions: e.g. enzyme-inducing AEDs can limit the effectiveness of oral contraception
Surgery: limited for refractory epilepsy: Removal of definable epileptogenic focus
What is Status Epilepticus?
A life-threatening neurological condition defined as 5 or more minutes of either continuous seizure activity or repetitive seizures without regaining consciousness
What is the management for Status Epilepticus?
Treatment is often initiated in 5–10 minutes as early treatment has higher treatment success (definition is >30 mins)
1. Resuscitate and protect airway, breathing and circulation
2. Check glucose and give if hypoglycaemic- consider thiamine
3. IV lorazepam or IV or PR diazepam (repeat once after 15 min if needed)
If seizures recur or fail to respond, IV phenytoin (15mg/kg) under ECG monitoring
Alternative IV agents include phenobarbitone, levetiracetam or sodium valproate
4. If these measures fail, consider general anaesthesia. This requires intubation and mechanical ventilation
5. Treat the cause: e.g. correct hypoglycaemia or hyponatraemia
6. Check plasma levels of all anticonvulsants
What are the complications of Epilepsy?
Fractures with tonic-clonic seizures
Behavioural problems
Sudden death in epilepsy (SUDEP)
Complications of AEDs (e.g. neutropenia or osteoporosis with carbamazepine)
What is the prognosis of Epilepsy?
50% remission at 1 year
Mortality 2 in 100 000/year, directly related to seizure or secondary to injury
What is an Extradural Haemorrhage?
An acute bleed between the dura mater and the inner surface of the skull- also known as haematomas
What is the aetiology of Extradural Haemorrhage?
Most commonly caused by skull trauma in the temporoparietal area, usually following falls, assaults or sporting injuries
The pterion is vulnerable to trauma as it is the fusion point between the parietal, frontal, sphenoid and temporal bones: the middle meningeal artery is involved in 75% of EDH as it lies underneath the pterion, which leads to a high risk of arterial rupture
What is the epidemiology of Extradural Haemorrhage?
Patients most commonly affected are adult males between 20-30 years old because they are more likely to experience a traumatic injury
What are the presenting symptoms of Extradural Haemorrhage?
Early signs:
- Severe headache: occurs after the initial impact and can persist
- Initial loss or fluctuance in consciousness: may present vaguely as tiredness or confusion
Period of lucidity after initial loss of consciousness: usually lasts between 6 and 8 hours but may last for days depending on the speed of the haematoma growth
Late signs:
Rapid deterioration and loss of consciousness:GCS score will begin to drop as intracranial pressure rises and the brainstem begins to herniate
What are the signs of Extradural Haemorrhage on physical examination?
Eyes:
- Focal neurological deficits become apparent in the eyes due to compression of the cranial nerves
- E.g. CNIII (oculomotor nerve) palsy may result in fixed dilation of the ipsilateral pupil. This is colloquially known as a “blown pupil”
Muscle weakness:
- Hemiparesis typically begins on the contralateral side to the EDH due to compression of the ipsilateral motor cortex
- Hemiparesis may become bilateral as the ICP increases and the brainstem becomes compressed
- Ipsilateral hemiparesis can also occur through Kernohan’s phenomenon (extensive midline shift of the brain due to mass effect from the growing extradural haematoma)
Upper motor neuron signs:
-Positive Babinski’s sign (upgoing toes), hyperreflexia and spasticity (hypertonia)
(signs are not specific to EDH)
Cushing’s triad:
A physiological response to critically high ICP
This is characterised by bradycardia, hypertension and deep/irregular breathing
Persisting unconsciousness: deep coma and very low GCS
Death: often by respiratory arrest
due to compression of the respiratory centres in the brainstem so they are unable to function
What are the appropriate investigations of Extradural Haemorrhage?
Non-contrast CT: FIRST LINE
- Show characteristic bi-convex mass within the skull if there is an EDH is present (“lemon-shaped” )
- Occurs as because the dura attaches to the skull more tightly across the suture lines and the pressure of the haematoma is not enough to overcome these sutures
- Secondary features on CT head can include midline shift and brain stem herniation, both of which are indications for early surgical intervention
MRI/X-ray: can also be performed but not as sensitive as CT. Show bone fractures and MRI can help differentiate between extradural and subdural haemorrhages through looking at the displaced dura
*Lumbar punctures are absolutely contraindicated for extradural haematomas, as they result in a drop in CSF pressure, which may speed up brain herniation
What is a head injury?
Any sort of injury to your brain, skull, or scalp. This can range from a mild bump or bruise to a traumatic brain injury. Common head injuries include concussions, skull fractures, and scalp wounds
Can be either closed or open (penetrating)- through the skull
What is the aetiology of head injuries?
Accidents at home, work, outdoors, or while playing sports
Falls (the most common cause of a skull fracture is a fall from a height)
Physical assault
Traffic accidents
What is the epidemiology of head injuries?
The most common causes in:
-Infants are falls and abuse
-Older children are falls and traffic accidents
-Adults are falls, followed by traffic accidents, followed by assaults
Skull fractures occur in 2% to 20% of all head trauma
Occur most frequently between the ages of 20 and 50 years
Men are more commonly affected
*Children with a head injury have an increased prevalence of skull fracture
What are the presenting symptoms of a head injury?
Loss of consciousness (few seconds to a few minutes) No loss of consciousness, but a state of being dazed, confused or disoriented Headache Nausea or vomiting Fatigue/drowsiness Problems with speech Difficulty sleeping or sleeping more than usual Dizziness or loss of balance Blurred vision Tinnitus Change in taste/smell Sensitivity to light or sound Memory/concentration difficulties Mood changes
What are the signs of a head injury on physical examination?
GCS: altered mental state
Evidence of trauma- bleeding, bruises
Abnormal pupillary reflexes- suggest herniation or brainstem injury
Conductive hearing loss
Open fracture- Laceration or wound to skin/soft tissue with exposed fractured bone or visible bone fragments
Periorbital ecchymoses. Battle’s sign: bleeding underneath the skin
What are the appropriate investigations for a head injury?
1st: Cranial CT: remains the imaging modality of choice: detects skull fractures and any associated intracranial pathology
If patients have a PMH of clotting or bleeding disorders, a CT should be performed within 8 hours
Others:
-MRI: Can be a useful adjunct or a secondary imaging modality, main benefit is increased detection of associated intracranial pathology such as diffuse axonal injury
-MR angiography: detects any associated vascular injury/pathology e.g. carotid canal, superior sagittal sinus
-beta-2 transferrin assay:
For any patient with head trauma and otorrhoea /rhinorrhoea to detect a CSF leak
-Audiogram: conductive or sensorineural hearing loss
-Cranial ultrasound: benefit to be use adjunct to CT in children
-Skeletal scan
What is Ischaemic heart disease?
Characterized by reduced blood supply (ischaemia) to the heart muscle resulting in chest pain known as angina pectoris. Can present as:
- Stable angina
- Acute coronary syndrome (ACS)
What can Acute coronary syndrome (ACS) be divided into?
Unstable angina (no cardiac injury)
Non-ST-elevation myocardial infarction (NSTEMI)
ST-elevation MI (STEMI, transmural infarction)
*MI refers to cardiac muscle necrosis resulting from ischaemia
What is the aetiology of angina pectoris?
Occurs when myocardial oxygen demand exceeds oxygen supply
The most common cause is atherosclerosis
Other causes of coronary artery narrowing are: RARE
-Spasm (e.g. from cocaine)
-Arteritis
-Emboli
What is the aetiology of a myocardial infarction?
Caused by sudden occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation
What is the aetiology of atherosclerosis?
- Endothelial injury
- Migration of monocytes into subendothelial space and differentiation into macrophages
- Macrophages accumulate LDL lipids in the subendothelium and become foam cells
- They release growth factors, which stimulate smooth muscle proliferation, production of collagen and proteoglycans
- This leads to the formation of an atheromatous plaque
What are the risk factors for Ischaemic heart disease?
Male Diabetes mellitus FH of MI Hypertension Hyperlipidaemia Smoking PMH MI
What is the epidemiology of Ischaemic heart disease?
Common, prevalence is >2%
More common in males
Annual incidence of MI in the United Kingdom is 5 in 1000
What are the presenting symptoms of Acute Coronary Syndrome?
Chest pain or discomfort of acute onset
Central heavy tight ‘gripping’ pain that radiates to arms (usually left), neck, jaw or epigastrium
Occurring at rest, increased severity and frequency of previously stable angina
Associations:
-Breathlessness
-Sweating
-Nausea and vomiting
Can be silent in elderly or in patients with diabetes
What are the presenting symptoms of stable angina?
Chest pain bought on by exertion and relieved by rest
What are the signs of acute coronary syndrome on physical examination?
May have no clinical signs
Pale, sweating, restless, low-grade pyrexia
Check both radial pulses for aortic dissection
Arrhythmias, disturbances of BP
New heart murmurs (e.g. pansystolic murmur of mitral
regurgitation from papillary muscle rupture or ventricular septal defect)
Signs of complications, i.e. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oliguria)
What are the appropriate investigations for Ischaemic heart disease?
Bloods: FBC, U&Es, CRP, glucose, lipid profile, cardiac enzymes:
-CK-MB and troponin-T or I1 (sensitive marker of cardiac injury, increase after 12 h), amylase (pancreatitis may mimic MI), TFTs. AST and LDH increase after 24 and 48 h, respectively; occasionally used only to make retrospective diagnosis
ECG:
Unstable angina or NSTEMI:
-May show ST depression, T-wave inversion (Q waves in these patients may indicate old MIs)
-ST-elevation (Q-wave)
MI:
-Hyperacute T waves, ST elevation (>1 mm in limb leads, >2 mm inchest leads), new-onset LBBB
-Later: T inversion (hours) and Q waves (days)
CXR: To look for signs of heart failure.
Exercise ECG testing (treadmill test)2: To determine prognosis and management (for patients with troponin-negative ACS, or stable angina with an intermediate or
high pretest probability of coronary heart disease)
Radionuclide myocardial perfusion imaging (rMPI):
Can be performed under stress (exercise or pharmacological) or at rest
*Stress testing would show low uptake in ischaemic myocardium
Rest testing can be used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs
Echocardiogram:
- Measure LVEF (early measurements may be misleading because of myocardial stunning)
- Exercise (or dobutamine stress) echocardiography may detect inducible wall motion abnormalities
Pharmacologic stress testing:
- For patients who cannot exercise or if the exercise test is inconclusive. Pharmacological agents such as dipyridamole, adenosine or dobutamine can be used to induce a tachycardia
- Various imaging modalities (e.g. rMPI, echocardi- ography) can be used to detect ischaemic myocardium. *Dipyridamole and adenosine are contraindicated in AV block and reactive airway disease
Cardiac catheterization/angiography:
In ACS with positive troponin or if high risk on stress testing
What is the management of stable angina?
Minimize cardiac risk factors:
-Control BP, hyperlipidaemia and diabetes. Provide advice onsmoking, exercise, weight loss and low-fat diet. *All patients should receive aspirin (75 mg/ day) unless contraindicated
Immediate symptom relief:
-GTN as a spray or sublingually.
Long-term treatment:
b-Blockers, e.g. atenolol, unless contraindicated (contraindications include acute heart failure, cardiogenic shock, bradycardia, heart block, asthma), calcium channel blockers (e.g. verapamil, diltiazem), nitrates (e.g. isosorbide dinitrate). Dual therapy may be indicated if monotherapy is ineffective
Percutaneous coronary intervention (PCI):
For localized areas of stenosis, in patients with angina not controlled despite maximal tolerable medical therapy Re-stenosis rate is 25% at 6 months
Coronary artery bypass graft (CABG): For more severe cases (three-vessel disease). The rates of MI and overall survival are generally similar between PCI and CABG
What is the management for Unstable angina/NSTEMI?
Admit to coronary care unit (CCU), oxygen, IV access, monitor vital signs and serial ECG
- Analgesia: GTN (initially sublingual, IV infusion if persistent chest pain), morphine sulphate/
diamorphine, antiemetic (metoclopramide).
- Aspirin (loading): 300 mg chewed. Maintenance: 75 mg, indefinite.
- Clopidogrel (loading-anti-platelet): 300 mg. Maintenance: 75 mg for at least 1 year if troponin positive or high risk
- Low-molecular-weight heparin (e.g. enoxaparin or dalteparin).
- b-Blocker (e.g. metoprolol) if not contraindicated.
- Glucose–insulin infusion if blood glucose >11 mmol/L.
- Consider glycoprotein (GP) IIb/IIIa inhibitors, e.g. tirofiban in patients:
. undergoing PCI; or
. at high risk for further cardiac events (troponin positive, TIMI risk score 4, continuingischaemia or other high-risk features)
*If little improvement, consider urgent angiography with revascularization
What is the management for a STEMI?
Admit to CCU, oxygen, IV access, monitor vital signs and serial ECG.
- Analgesia: GTN
- Aspirin (loading): 300 mg chewed.
- Clopidogrel (loading): 600 mg if patient going to primary PCI, 300 mg if undergoing thrombolysis and 75 years of age, 75 mg if undergoing thrombolysis and >75 years of
age. Maintenance: 75 mg, for at least 1 year
- b-Blocker (e.g. metoprolol)
- If undergoing primary PCI: IV heparin (plus GP IIb/IIIa inhibitor) or bivalirudin (an antithrombin). If undergoing thrombolysis with recombinant tissue plasminogen
activator (rtPA): IV heparin.
- Glucose–insulin infusion if blood glucose >11 mmol/L
-Primary PCI
-Thrombolysis: Using fibrinolytics such as streptokinase or rtPA (alteplase, reteplase,tenecteplase) if within 12h of chest pain with ECG changes (ST elevation, new-onset LBBB or posterior infarction) and not contraindicated.
Rescue PCI: If continued pain or ST elevation after thrombolysis (<50% decrease of the initial ST-segment elevation on a follow-up ECG 60–90 min after fibrinolytic therapy)
What are the other managements for Ischaemic heart disease?
Secondary Prevention:
-Antiplatelet agents (aspirin and clopidogrel)
-ACE inhibitors, b-blockers and statins
-Control other risk factors (smoking, diabetes, hypertension)
Advice:
Not to drive for 1 month following MI
Education by cardiac rehabilitation team:
-lifestyle changes (e.g. exercise, stop smoking, changing diet)
CABG for patients with left main stem or three-vessel disease
What are the complications of Ischaemic heart disease?
At risk of MI and other vascular diseases (e.g. stroke, peripheral vascular disease) Cardiac injury can lead secondarily to heart failure and arrhythmias Early complications of MI (24–72 h): -Death -Cardiogenic shock -Heart failure -Ventricular arrhythmias -Heart block -Pericarditis -Myocardial rupture -Thromboembolism Late complications of MI: -Ventricular wall (or septum) rupture -Valvular regurgitation -Ventricular aneurysms -Tamponade -Dresslers syndrome (pericarditis) -Thromboembolism
What is the prognosis of Ischaemic heart disease?
ACS: TIMI score (range 0–7) can be used for risk stratification (high scores are associated with high risk of cardiac events within 30 days), consists of:
(1) >65 years;
(2) known coronary artery disease;
(3) aspirin in last 7 days;
(4) severe angina (>2 episodes in 24 h); (5) ST deviation >1 mm;
(6) elevated troponin levels;
(7) >3 coronary artery disease risk factors
(hypertension, hyperlipidaemia, family history, diabetes, smoking)
Killip classification of acute MI:
Class I: no evidence of heart failure.
Class II: mild to moderate heart failure (S3, crepitations
What is Meningitis?
Inflammation of the meninges (pia mater and arachnoid) (coverings of the brain) most commonly caused by infection
What is the aetiology of Meningitis?
Infection:
Bacterial:
-Neonates: Group B streptococci, Escherichia coli, Listeria monocytogenes
-Children: Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae
-Adults: *Neisseria meningitidis (meningococcus), Streptococcus pneumoniae, TB
-Elderly: Streptococcus pneumoniae, Listeria monocytogenes
Viral: Enteroviruses, mumps, Herpes simplex V, HIV
Fungal: Cryptococcus (associated with HIV infection)
What are the risk factors for Meningitis?
Close communities (e.g. dormitories) Basal skull fractures Mastoiditis Sinusitis Inner ear infections Alcoholism Immunodeficiency Splenectomy Sickle cell anaemia CSF shunts Intracranial surgery
What is the epidemiology of Meningitis?
Variation according to geography, age, social conditions
Viral meningitis is one of the most common infections of the CNS
What are the presenting symptoms of Meningitis?
ASK ABOUT TRAVEL HISTORY *Severe headache *Photophobia *Neck stiffness or backache Irritability Drowsiness Vomiting Fever Clouding of consciousness High-pitched crying or fits (common in children)
What are the signs of Meningitis on physical examination?
Signs of meningism: -Photophobia -Neck stiffness Signs of infection: -Fever -Tachycardia -Hypotension -Skin rash (petechiae with meningococcal septicaemia) -Altered mental state
What are the appropriate investigations for Meningitis?
Blood: Two sets of blood cultures (do not delay antibiotics)
Imaging:
-CT scan to exclude a mass lesion or increased intracranial pressure before LP, (may lead to cerebral herniation during subsequent CSF removal)
*A CT scan of the head must be done before LP in patients with:
-Immunodeficiency
-History of CNS disease
-Reduced consciousness
-Fit
-Focal neurologic deficit
-Papilloedema
Lumbar puncture: Send CSF for MCS and Gram staining (Streptococcus pneumoniae: Gram-positive diplococcic, Neisseria Meningitidis: gram-negative diplococcic)
Bacterial: Cloudy CSF, raised neutrophils, raised protein, reduced glucose (CSF: serum glucose ratio of <0.5)
Viral: raised Lymphocytes, raised protein BUT normal glucose
*TB: Fibrinous CSF, raised lymphocytes, raised protein, reduced glucose
What is the management for Meningitis?
Immediate IV/IM antibiotics if meningitis suspected (before lumbar puncture or CT)
Antibiotics:
Benzylpenicillin may be given as initial blind therapy
Amoxicillin + gentamicin
Add vancomycin and if necessary rifampicin
If anaphylaxis to penicillin or cephalosporins- use chloramphenicol
Steroids:
IV (10 mg for 4 days) given shortly before or with first dose of antibiotics to reduce complications
Avoid dexamethasone in patients with HIV
Resuscitation: Patient is best managed in ITU
Prevention (only applicable to meningococcal meningitis): Notify public health services and consult a consultant in communicable disease control, vaccination for meningococcal serogroups A and C
What are the complications for Meningitis?
Septicaemia Shock DIC-disseminated intravascular coagulation, which is the inappropriate clotting of blood within the vessels Renal failure Fits Peripheral gangrene Cerebral oedema Cranial nerve lesions Cerebral venous thrombosis Hydrocephalus Water- house–Friderichsen syndrome (bilateral adrenal haemorrhage)
What is the prognosis of Meningitis?
Mortality rate from bacterial meningitis is high (10–40% with meningococcal sepsis)
In developing countries mortality rate often higher
Viral meningitis self-limiting
What is Multi-organ dysfunction syndrome?
The presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention
Defined as severe pain associated with failure of at least two of the following organs: liver, lung, and kidney
What is the aetiology of Multi-organ dysfunction syndrome?
Widespread vaso-occlusion is thought to be responsible
What is the epidemiology of Multi-organ dysfunction syndrome?
Often associated with severe pain in patients with previously mild disease and a relatively high haemoglobin
Death has been reported in up to 25% of patients
What are the presenting symptoms and signs of Multi-organ dysfunction syndrome on physical examination?
An atypically severe vaso-occlusion
Fever
Sudden deterioration including a drop in Hgb and platelets
Diffuse encephalopathy
Rhabdomyolysis- breakdown of damaged skeletal muscle
What are the appropriate investigations for Multi-organ dysfunction syndrome?
The multiple organ dysfunction score:
Using physiological variables to determine the level of dysfunction
-Resp: PO2/FiO2 ratio
-Renal: serum creatinine
-Hepatic: serum bilirubin
-Cardiovascular: pulmonary artery to aorta ratio
-Haematological: platelets
-Neurological: GCS
What are the clinical features of Multi-organ dysfunction syndrome?
Lung: failure of normal gas exchange, reflected predominantly in arterial hypoxemia
Kidney: reflected in impairment of normal selective excretory function, initially in oliguria despite adequate intravascular volume, but later in a rising creatinine level, and fluid and electrolyte derangements of sufficient magnitude that dialysis is required
Liver: hyperbilirubinemia and cholestasis (reduction or stoppage of bile flow)
What is Opioid Overdose?
An opioid is any synthetic or natural agent that stimulates opioid receptors and produces opium-like effects. Opiates are opioids naturally derived from the opium poppy, Papaver somniferum, and include morphine and codeine
An overdose occurs when larger quantities than physically tolerated are taken, resulting in:
-CNS and respiratory depression
-Miosis
-Apnoea
which can be fatal if not treated rapidly
What is the aetiology of Opioid Overdose?
Substance abuse in regular users/abusers of illicit or prescription opioids
Unintentional overdose in patients prescribed opioids for pain by taking larger amounts than tolerated
Intentional overdose and intent of self-harm (suicidality)
Therapeutic drug error; iatrogenic overdose by a practitioner unfamiliar with opioid prescribing, or an adverse drug reaction
What is the epidemiology of Opioid Overdose?
Opioid abuse and overdose is a growing problem worldwide
Common cause of death in prisoners one released due to loss of tolerance
What are the presenting symptoms of Opioid Overdose?
*Miosis (constricted pupils)
Altered mental state
Fresh needle marks
Old tracks on arms and legs
What are the signs of Opioid Overdose on physical examination?
Miosis (constricted pupils)
Bradypnoea: respiratory rate of <12 breaths/minute
Altered mental state
Fresh needle marks
Old tracks on arms and legs
What are the appropriate investigations for Opioid Overdose?
*Dramatic response to naloxone: diagnostic of opioid overdose
ECG: In patients with significant respiratory compromise, look for abnormal ECG (e.g. signs of myocardial ischaemia)
Others:
-CXR: Indicates acute respiratory distress syndrome (non-cardiogenic pulmonary oedema): perihilar, basilar, or diffuse alveolar infiltrates
-Gas chromatography/ mass spectrometry: most sensitive and specific but not useful in opioid overdose due to long turn over time
What is Paracetamol Overdose?
Excessive ingestion of paracetamol causing toxicity
What is the aetiology of Paracetamol Overdose?
Maximum recommended dose: 2x 500 mg tablets 4 times in 24 h
Intake of > 12 g or > 150 mg/kg can cause hepatic necrosis
What is the epidemiology of Paracetamol Overdose?
Most common intentional drug overdose in the United Kingdom, 70,000/year
Women more than men
Causing 100 deaths/year-reduced by legislation in 1998 restricting pack sizes
What are the associations/risk factors for Paracetamol Overdose?
Commonly associated with ingestion of other substances, e.g. alcohol
Patients on enzyme-inducing drugs (which increase cytochrome P450 activity, e.g. anticonvulsants or anti-TB drugs)
Malnourished
Anorexia nervosa
HIV
These patients are more susceptible to toxic effects of paracetamol
What are the presenting symptoms of Paracetamol Overdose?
Very important to ascertain timing and quantity of overdose, and presence of risk factors
0–24 h: Asymptomatic or mild nausea, vomiting, lethargy, malaise
24–72 h: RUQ abdominal pain, vomiting
> 72 h: Increasing confusion (encephalopathy), jaundice
What are the signs of Paracetamol Overdose on physical examination?
0–24 h: No signs are evident
24–72 h: Liver enlargement and tenderness
> 72 h: Jaundice, coagulopathy, hypoglycaemia and renal angle pain
What are the appropriate investigations for Paracetamol Overdose?
Serum paracetamol levels:
-4 h post ingestion (absorbed rapidly, hence peak plasma levels are usually within 4h)
Bloods:
-Serum AST and ALT: elevated
-U&Es: may show renal impairment
-Serum prothrombin time and INR: PT may be prolonged and INR may be increased
-Lactate and ABG (for degree of acidosis): monitor severity of hepatic failure
What is the pathogenesis of Paracetamol Overdose?
At therapeutic levels, paracetamol is metabolized in the liver by conjugation with glucuronate or sulphate and excreted by the kidneys A proportion (< 7 %) is metabolized by cytochrome P450 oxidase to form a toxic highly reactive intermediate N-acetyl-p-benzoquinoneimine (NAPQI) This intermediate can be inactivated by conjugation with glutathione
At toxic levels the conjugation pathway and glutathione stores are overwhelmed, and so there is a build up of this toxic intermediate
This leads to NAPQI-induced oxidative damage and acute liver necrosis
What is given to patients with Paracetamol Overdose?
Antidote should be given: IV N-acetylcysteine (NAC)
What is a Stroke?
The rapid permanent neurological deficit from cerebrovascular insult
Also defined clinically, as focal or global impairment of CNS function developing rapidly and lasting >24 h
What is a Transient Ischaemic Attack (TIA
A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction, fully resolving within 24h
What can Stroke be divided into?
Ischaemic (caused by vascular occlusion or stenosis)
Haemorrhage (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage)
What is the aetiology of an Ischaemic Stroke?
87% of strokes are Ischaemic
Causes include:
Thrombosis:
-In the elderly, this arises from atherosclerosis within cerebral vessels affecting mainly small vessels (causing lacunar infarcts) and less commonly large vessels (e.g. middle cerebral artery)
-Can also arise from prothrombotic states (e.g. dehydration or thrombophilia).
Emboli:
-From intimal flap of carotid dissection, atheromatous plaques in the carotid arteries or from the heart (e.g. atrial fibrillation)
Hypotension:
-If below the autoregulatory range maintaining cerebral blood flow, infarction results in the watershed zones between different cerebral artery territories
Others: Vasculitis, cocaine
What is the aetiology of a Haemorrhagic Stroke?
Around 10% of cases Hypertension -Charcot–Bouchard microaneurysm rupture Amyloid angiopathy Arteriovenous malformations Less commonly: trauma, tumours, arteriovenous malformations, vasculitis
What is the epidemiology of Stroke?
Common Annual incidence is 2 in 1000 Third most common cause of death in industrialized countries (US, UK) Most patients are in seventh decade Young strokes (<50 years merit extensive investigation) Ischaemic -87% Haemorrhagic -10% Subarachnoid haemorrhage -3%
What are the presenting symptoms of a Stroke?
*Sudden onset (deterioration within seconds)
*Weakness, sensory, visual or cognitive impairment, impaired coordination, or consciousness
Unilateral
Head or neck pain (in carotid or vertebral artery dissection)
*Enquire time of onset (critical for emergency management if <4.5 h)
Enquire if history of atrial fibrillation, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain
What are the signs of an Ischaemic Stroke on physical examination?
Anterior circulation
- Anterior cerebral: Lower limb weakness (motor cortex), confusion (frontal lobe)
- Middle cerebral: Facial weakness, hemiparesis (motor cortex), hemisensory loss (somatosensory cortex), apraxia, hemineglect (parietal lobe), receptive or expressive dysphasia (language centres), quadrantanopia (superior or inferior optic radiations)
Posterior circulation
- Posterior cerebral: Hemianopia (blindness over half the visual field)
- Anterior inferior cerebellar artery: Vertigo, ipsilateral ataxia, ipsilateral deafness (or tinnitus), ipsilateral facial weakness
- Posterior inferior cerebellar artery (lateral medullary syndrome of Wallenberg): Vertigo, ipsilateral ataxia, ipsilateral Horners syndrome, ipsilateral hemifacial sensory loss, dysarthria and contralateral spinothalamic sensory loss
- Basilar artery: Combination of cranial nerve pathology and impaired consciousness (emergency)
What are the signs of Lacunar Infarcts on physical examination?
Disease in the deep perforating arteries:
- Internal capsule or pons: Pure sensory or motor deficit (or combination of both)
- Thalamus: Loss of consciousness, hemisensory deficit
- Basal ganglia: Hemichorea, hemiballismus (movement disorder), Parkinsonism
Multiple lacunar infarcts:
- Vascular dementia
- Urinary incontinence
- Gait apraxia (marche a petits pas, shuffling small-stepped gait, with upright posture and often normal or excessive arm-swing)
What are the signs of a Haemorrhagic Stroke on physical examination?
Headache Meningism Focal neurological signs Nausea and vomiting Signs of raised ICP (papilloedema) Seizures
What are the appropriate investigations for Stroke?
Protect the airway: This avoids hypoxia/aspiration
Maintain homeostasis:
-Blood glucose: keep between 4–11 mmol/L
URGENT CT/MRI within 1h:
(1st)CT-head: For rapid detection of haemorrhages- often normal especially in lacunar infarcts or very early in the stroke (<6 h)
MRI-brain: Rarely available acutely, but much higher sensitivity for infarction
Diffusion-weighted imaging (DWI) can differentiate between recent strokes (<2 weeks) and old strokes
-Essential if: thrombolysis considered, high risk of haemorrhage (reduced GCS, signs of high ICP, severe headache, meningism, progressive symptoms, bleeding tendency or anticoagulated)
Others:
- ECG: exclude arrhythmia or ischaemia
- Carotid Doppler ultrasound: Important to exclude carotid artery disease.
- CT-cerebral angiogram: To detect artery dissections or intracranial stenosis
- Cardiac enzymes: exclude concomitant MI
- Prothrombin time: if no DH of anticoagulant use then thrombolysis does not need to be delayed for test results
What does FAST stand for in an acute stroke setting?
F- facial dropping
A- arm weakness
S- speech difficulties
T- time (narrow therapeutic window as stroke is a permanent condition)
What is the management for a hyperacute (<4.5h) Ischaemic Stroke?
*If haemorrhage excluded on CT-head:
Intravenous thrombolysis may be considered (Alteplase)
*best results are within 90 minutes
What is the management for an Ischaemic Stroke?
- Aspirin or clopidogrel to prevent further thrombosis once haemorrhage excluded on CT-head.
- Heparin anti-coagulation may be considered in certain subgroups where there is a high risk of emboli recurrence or stroke progression (e.g. carotid dissection, recurrent cardiac emboli, critical carotid artery stenosis)
- Formal swallow assessment is essential (nasogastric tube may be required)
- Close nursing and GCS monitoring
- Thromboprophylaxis (graded compression stockings)
- Hemicraniectomy may be indicated for mass effect from infarcted tissue in the first 48 h
*Multidisciplinary rehabilitation: Speech and language
therapy, occupational therapy, physiotherapy and neuropsychology.
What is the management for a Haemorrhagic Stroke?
Control hypertension and seizures
IV mannitol and hyperventilation helps lower intracranial pressure
Evacuation of haematoma or ventricular drainage may be required
*Multidisciplinary rehabilitation: Speech and language
therapy, occupational therapy, physiotherapy and neuropsychology.
What is the secondary prevention in Strokes?
Aspirin and dipyridamole, warfarin anticoagulation (if atrial fibrillation), stop smoking, control hypertension and hyperlipidaemia, treatment of carotid
artery disease
What is the surgical treatment of Strokes?
Carotid endartectomy within 2 weeks of stroke or TIA reduces risk of further stroke although carries a significant peri-operative risk
- symptomatic stenosis of 70–99% or
- symptomatic stenosis of 50–99% or
- crescendo TIAs not responding to medical treatment
What are the complications of Stroke?
Cerebral oedema (raised ICP and local compression)
Immobility
Infections (e.g. pneumonia, UTI, from pressure sores) DVT
Cardiovascular events (arrhythmias, MI, cardiac failure)
Death
What is the prognosis for Stroke?
10% mortality in first month
Up to 50% of those who survive remain dependent
10%have a recurrence in 1 year
Generally, poorer for haemorrhage than for ischameic.
What is a Subarachnoid Haemorrhage?
Arterial bleeding into the subarachnoid space and is a medical emergency
What is the aetiology of Subarachnoid Haemorrhage?
Rupture of an intracranial saccular aneurysm is the leading cause of non-traumatic SAH, accounting for approximately 80% of cases (usually at Circle of Willis)
The remaining 20% are attributed to non-aneurysmal perimesencephalic SAH, arteriovenous malformations, arterial dissections, use of anticoagulants, drug abuse (e.g. cocaine, amphetamines) and other rare conditions
What is the epidemiology of Subarachnoid Haemorrhage?
Peak age of incidence in the fifth decade
3% of all cases of Stroke
What are the risk factors/associations of Subarachnoid Haemorrhage?
Hypertension Smoking Excess alcohol intake Saccular aneurysms are associated with: -polycystic kidney disease Marfans syndrome -pseudoxanthoma elasticum (genetic disease that causes mineralization of elastic fibers in some tissues, can cause premature atherosclerosis) -Ehlers–Danlos syndrome (connective tissue disorder)
What are the presenting symptoms of Subarachnoid Haemorrhage?
Sudden onset severe headache (classically described as 'THUNDERCLAP HEADACHE') Nausea and vomiting Neck stiffness Photophobia Reduced level of consciousness
What are the signs of Subarachnoid Haemorrhage on physical examination?
Meningism:
-Neck stiffness
-Kernigs sign (resistance or pain on knee extension when hip is flexed) because of irritation of the meninges by blood
-Pyrexia
Reduced GCS
Signs of increased intracranial pressure:
-Papilloedema
-IV or III cranial nerve palsy, ophthalmoplegia
-Hypertension and bradycardia.
Fundoscopy:
-Rarely subhyaloid haemorrhage (between retina and vitreous membrane)
Focal neurological signs:
Usually develop on second day and are caused by ischaemia from vasospasm and reduced brain perfusion
What are the appropriate investigations for Subarachnoid Haemorrhage?
*Order an emergency non-contrast CT head in all patients presenting with acute sudden, severe headache (thunderclap headache)- standard diagnostic test:
-Hyperdense areas in the basal regions of the skull (caused by blood in the subarachnoid space)
Bloods:
-FBC: Leukocytosis (cerebral vasospasm)
-U&Es: Hyponatraemia is the most common electrolyte abnormality in SAH
-Troponin I: elevated during first 24h, associated with poorer outcomes
-Serum glucose: Hyperglycaemia develops in 1/3 of SAH
-clotting: coagulopathy may be present
ECG: arrhythmias, ischaemia
Angiography (CT or intra-arterial):
-To detect the source of bleeding if the patient is a
candidate for surgery or endovascular treatment
Lumbar puncture:
-Raised opening pressure, increased red cells, few white cells, xanthochromia (straw-coloured CSF, bloody CSF) because of breakdown of Hb, confirmed by spectrophotometry of CSF
What is a Subdural haemorrhage?
A collection of blood that develops between the dural and arachnoid coverings of the brain
Acute: Within 72 h
Subacute: 3–20 days
Chronic: After 3 weeks
What is the aetiology of a Subdural haemorrhage?
The primary aetiology of both acute and chronic subdural haematomas is trauma
-results in shearing forces which tear veins (bridging veins) that travel from the dura to the cortex
Less commonly, subdural haematomas are associated with rupture of a cerebral aneurysm or vascular malformation
In children, non-accidental injury should always be considered
What is the epidemiology of Subdural haemorrhages?
Acute: Tend to occur in younger patients/associated with major trauma (5–25% of cases of severe head injury)
More common than extradural haemorrhage
Chronic: More common in elderly, studies report incidence of 1–5 per 100 000
What are the presenting symptoms of a Subdural haemorrhage?
Acute: -History of trauma with head injury -Patient has reduced conscious level Subacute: -Worsening headaches 7–14 days after injury, altered mental status Chronic: -Can present with: headache confusion cognitive impairment psychiatric symptoms gait deterioration focal weakness seizures *There may not be a history of fall or trauma; hence have low index of suspicion especially in the elderly and alcoholics
What are the signs of a Subdural haemorrhage on physical examination?
Acute:
-Reduced GCS
-With large haematomas resulting in midline shift, an ipsilateral fixed dilated pupil may be seen (compression of the ipsilateral third nerve parasympathetic fibres)
-Pressure on brainstem: reduced consciousness, bradycardia
Chronic:
-Neurological examination may be normal
-There may be focal neurological signs (III or VI nerve dysfunction, papilloedema, hemiparesis or reflex asymmetry)
What are the appropriate investigations for a Subdural haemorrhage?
*Non-contrast CT scan: ‘lemon’ shaped (crescent) mass, concave over brain surface
-CT appearance changes with time
-Acute subdurals are hyperdense, becoming isodense over 1–3 weeks (such that presence may be inferred from signs such as effacement of sulci, midline shift, ventricular compression and obliteration of basal cisterns)
-Chronic subdurals are hypodense (approaching that of CSF)
MRI-brain: Has higher sensitivity especially for isodense or small SDHs
Plain x-ray: skull fracture
What is the management for Subdural haemorrhages?
Acute:
ALS protocol with priorities of cervical spine control and ABC (head injury has a significant risk of cervical spine injury)
Disability: GCS, pupillary reactivity
Antiplatelet or anticoagulant agent stopped and/or reversed
If signs of raised ICP, head elevation and consider osmotic diuresis with mannitol and/or hyperventilation
Once stabilised, obtain CT-head
Conservative:
Especially if small and minimal midline shift (SDH<10mm thickness, and midline shift <5 mm)
Surgical:
Prompt Burr hole or craniotomy and evacuation for symptomatic subdurals >10 mm, with >5 mm midline shift (better outcome if within 4 h)
ICP monitoring devices may be placed
Chronic:
- If symptomatic or there is mass effect on imaging, surgical treatment with Burr hole or craniotomy and drainage (a drain may be left in for 24–72 h)
- Asymptomatic SDH without significant mass effect is best managed conservatively with serial imaging to monitor for spontaneous resorption
- Haematomas that have not fully liquefied may require craniotomy with membranectomy
Children: Younger children may be treated by percutaneous aspiration via an open fontanelle or if this fails, placement of a subdural to peritoneal shunt
What are the complications of a Subdural haemorrhage?
Raised ICP
Cerebral oedema pre-disposing to secondary ischaemic brain damage
Mass effect (transtentorial or uncal herniation)
Post-op:
- Seizures are relatively common
- Recurrence (Up to 33% for SDH)
- Intracerebral haemorrhage
- Subdural empyema: a collection of pus, in the subdural space
- Brain abscess or meningitis
- Tension pneumocephalus: life threatening neurosurgical emergency, subdural air causes a mass-effect over the underlying brain parenchyma
What is the prognosis for a Subdural haemorrhage?
Acute: Underlying brain injury is the most important factor on outcome
Chronic: Generally have a better outcome than acute SDHs, reflecting lower incidence of underlying brain injury, with good outcomes in 3/4 of those treated by surgery
What is a urinary catheterisation?
A flexible tube used to empty the bladder and collect urine in a drainage bag
What are the indications for urinary catheterisation?
When people have difficulty urinating naturally. It can also be used to empty the bladder before or after surgery and to help perform certain tests
Obstruction in the urethra e.g. scarring or prostate enlargement
Bladder weakness or nerve damage that affects your ability to urinate
Drain bladder during childbirth- epidural anaesthetic
Drain bladder before, during or after some types of surgery
Deliver medicine directly into the bladder, such as during chemotherapy for bladder cancer
A last resort treatment for urinary incontinence when other types of treatment have been unsuccessful
What are the possible complications for a urinary catheterisation?
Main complications are UTIs (treated with antibiotics)
Others: bladder spasms, leakages, blockages, and damage to the urethra
