Acute Medicine Flashcards
What is the initial assessment and management of ACS?
300mg PO aspirin 300mg PO clopidogrel Diamorphine 2.5-10mg Metoclopramide 10mg IV GTN spray two puffs High flow oxygen Secure IV access 12 lead ECG FBC, glucose, troponin, lipids CXR to asses cardiac size and pulmonary oedema General examination
What conditions mimic pain in ACS?
Pericarditis Aortic dissection Pulmonary embolism Oesophageal reflux, spasm, rupture Biliary tract disease Perforated peptic ulcer Pancreatitis
What ECG changes are indicative of STEMI?
ST elevation
Pathological q waves (deep q waves) - indicate abnormal electrical conduction
ST depression is seen in leads reciprocal to the ST elevated leads
PR segment elevation/depression
When do serum Troponin levels rise and fall in STEMI?
Rise within 3-12 hours
Peak within 24-48 hours
Return to baseline over 5-14 days
Measure at presentation and at 10-12 hours after presentation
What are the indications for thrombolysis?
Cardiac pain within 12 hours and ST elevation in two contiguous ECG leads
Cardiac pain with new LBBB on ECG
Between what interval from the onset of chest pain should thrombolysis be administered?
Greatest benefit within four hours
Between 12-24 hours- thrombolysis if persisting symptoms and st elevation
What are common thrombolysis agents?
Streptokinase
Alteplase (rtPA) - use IV heparin as well
Reteplase
Tenecteplase
What are the complications and contraindications of thrombolysis?
Complications: Bleeding Hypotension Allergic reactions Intracranial haemorrhage
Contraindications: Internal bleeding Suspected aortic dissection Recent head trauma Previous haemorrhage stroke Trauma/surgery in last two weeks
What is the role of beta blockers and ACEI in STEMI?
Beta blockers:
Unless contraindicated
Use short acting agent IV eg metoprolol
Particularly of benefit in patients with tach arrhythmia, ongoing pain, hypertension
ACEI:
After aspirin, beta blockers and reperfusion, all patients with STEMI should receive ACEI in 24 hours
What is the gold standard for coronary reperfusion in STEMI?
PCI
Within 2 hours, 90 mins
What are the indications for PCI?
All patients with chest pain and st elevation or new LBBB
What is the difference between NSTEMI and unstable angina?
NSTEMI has evidence of myocardial damage, whereas unstable angina does not
How does NSTEMI/UA present?
Rest angina
New onset severe angina
Previously diagnosed angina which has become more frequent, longer in duration, or lower in threshold
How can NSTEMI/UA be diagnosed?
ECG changes:
ST depression
T wave inversion
Occasionally q waves or LBBB
Markers of cardiac injury:
A positive biochemical marker (CK, CKMB, troponin) with the aforementioned ECG changes is diagnostic of NSTEMI. If no changes in cardiac markers over 24-72 hours, UA is diagnosed
What agents are used to treat symptoms and for their anti-ischaemic effects in NSTEMI/UA?
Analgesia-Diamorphine 2.5-5mg IV- reduces pain and blood pressure
Nitrates - GTN infusion
B-blockers - start on presentation, shift acting metoprolol
Calcium antagonists- diltiazem/ verapamil to reduce hr and BP
Statins - atorvastatin - 80mg od
What anti platelet therapy is used in NSTEMI/UA?
Aspirin - 300mg administered indefinitely in emergency department - continue indefinitely
Clopidogrel - 300mg - continue on 75 mg for 12 months
What anti thrombotic therapy is used in NSTEMI/UA?
LMWH -
dalteparin/enoxaparin
Continue for 2-5 days after last episode of pain/ ECG changes?
Fondaparinux?
What are signs of severe haemodynamic compromise in bradyarrythmias?
And how should these be treated
Impending cardiac arrest
Severe pulmonary oedema
Blood pressure below 90
Depressed consciousness
Tachy - unsynchronised external defib
Brady - temporary pacing
How does atrial fibrillation typically present?
Palpitations Chest pain Breathlessness Collapse Hypotension Embolus - stroke, peripheral Asymptomatic Occur in 10-15% patients post MI
What is the curb 65 scoring system for pneumonia, and what actions should be taken for the different scores?
Confusion - amts less than/equal to 8 Urea - >7mmol Respiratory rate - greater than 30 BP - less than 90/60 Age - greater than 65
> 3- admit to hospital
2- increased risk of mortality- short inpatient stay
0-1- low risk, may be suitable for home treatment
What is the initial management and investigations for pneumonia
ABCDE Venous access, arrange for CXR Bloods- RBC, u+es, LFT, CRP ABG- give 02 if necessary Culture blood and sputum Pain relief- paracetamol and NSAID
More investigations if necessary Urine for legionella antigen Pleural fluid aspiration Mycoplasma cold agglutinins Bronchoscope and lab age if fail to respond
What is the empirical management of mild, moderate, severe CAP?
Mild moderate- amoxicillin plus clarithromycin or doxycycline
Severe - coamoxiclav IV plus clarithromycin IV
Or
Cefuroxime/cefotaxime IV plus clarithromycin IV
What is the empirical treatment of hospital acquired pneumonia
Cefotaxime IV with or without metronidazole IV
What is the empirical management of aspiration pneumonia?
Cefuroxime and metronidazole
Or Benzylpenicillin and gentamicin and metronidazole
What is the initial management of acute severe asthma attack?
Monitor PEFR and ABG
Sit patient up in bed
PEF is 33-50% predicted
(PEF <33% is life threatening)
High percentage O2 via reservoir mask
Nebulisers bronchodilators- 5mg salbutamol, repeat every 15-3ins if required
Add ipratropium bromide 0.5mg 4-6 hourly if initial response to salbutamol is poor
IV access
Steroids 200mg hydrocortisone IV
Antibiotics if evidence of chest infection
Adequate hydration
Consider IV magnesium, aminophylline, salbutamol infusion
What are the features of a mild- moderate asthma attack and how is it managed?
No severe features, pef 51-75% of predicted
Administer nebulised salbutamol 5mg and oral prednisolone 30-60mg
Reassess after 30 mins, if worse, treat as per severe asthma, if no better, repeat nebs
Discharge on oral prednisolone 30-40mg is for 7 days
Inhaled corticosteroid, inhaled beta agonist
What investigations should be ordered for acute exacerbation of COPD?
U+Es - dehydration, RF
FBC- leucocytosis, anaemia, secondary polycythaemia
ABG and pulsox
Sputum and blood culture
Peak flow- compare to what is normal for patient
CXR
ECG- check for mi or arrhythmia causing breathlessness
What is the management of acute exacerbation if COPD
Venturi mask O2 - 24-28% O2
ABG
If type 2 resp failure, consider NiV - CPAP or BIPAP, especially if failure to respond to bronchodilator therapy
Nebulised salbutamol 5mg
Consider IV salbutamol or aminophylline
Nebulised ipratropium bromide 500mcg 6 hourly
Steroids - 200mg hydrocortisone IV or 30-40mg prednisolone PO
Physio may help to clear bronchial secretions
What is the role if mechanical ventilation in acute exacerbation of COPD?
Ventilation should be considered where respiratory failure is present (paO2 less than 7.3) regardless of CO2 levels, and in those who fail to respond to first line treatment including bronchodilator therapy
Check with ITU staff!
Good outcome if young, good exercise tolerance, acute resp failure
Poor outcome if old, comirbidities, on O2 therapy at home
What is adult respiratory distress syndrome?
A common clinical disorder in which damage to the alveolar epithelial and endothelial barriers of the lung, acute inflammation, and protein rich pulmonary oedema leads to acute respiratory failure.
Often occurs in the setting of multiple organ failure
What are the diagnostic criteria for ARDS?
Acute onset of respiratory failure with one or more of the risk factors
Hypoxaemia- ALI- paO2:fiO2 ratio <19mmHG with normal colloid oncotic pressure
What investigations are appropriate in ARDS?
CXR ABG Blood, urine, sputum culture ECG Pulmonary artery catheter to measure pulmonary capillary wedge pressure, cardiac output
Which disorders are most associated with ARDS? Direct and indirect lung injury
Direct lung injury Aspiration Inhalation of smoke/noxious gases Pneumonia Pulmonary contusions Drug OD- O2, opiates, bleomycin, salicytes
Indirect lung injury Shock Septicaemia Pancreatitis Burns/ trauma Head injury and increased ICP Liver failure
How and where is ARDS most appropriately managed?
Usually HDU/ICU
Identify and treat underlying cause
Respiratory support to improve gas exchange and correct hypoxia- High O2 conc or mechanical ventilation
Cardiovascular support- arterial line, inotropes, fluid resus
What are causes of pneumothorax?
Primary/spontaneous- tall young men who smoke- rupture if apical subpleural blend
Secondary/spontaneous- pleural rupture due to underlying lung disease: emphysema, fibrosis etc
Infection- cavitating pneumonia
Trauma- chest trauma in RTA
Iatrogenic- mechanical ventilation, pleural biopsy, subclavian vein cannulation
What are signs of tension pneumothorax?
Distressed patient
Tachypnoeic with cyanosis
Profuse sweating
Marked tachycardia and hypotension
How may acute upper GI bleed present?
Haematemesis- bright red, dark clots, coffee grounds
Malaena- from anywhere proximal to caecum
Weakness, sweating, palpitations
Postural dizziness, fainting
Collapse or shock
What are causes of acute upper GI bleeding?
Peptic ulcer Gastroduodenal erosions Oesophagitis Varices Malory Weiss tear Upper GI malignancy Vascular malformations
What factors indicate a high risk of death in acute upper GI bleed, and what scoring system incorporates these?
Rockall scoring system
Age greater than 60 Shock - SBP 100 Comorbidities- cardiac, renal, liver, malignancy Diagnosis of GI tract malignancy Blood in upper GI tract
What is the initial management of acute upper GI bleeding?
Position patient on side to protect the airway
Secure IV access
Take FBC and U+E, platelets and LFTs, clotting and crossmatch
Fluid resus
Monitor urine output
IV PPI - 80mg omeprazole bolus, followed by 8mg/hr infusion
Contact on call endoscopy team and surgeons
What general measures can be taken to stop bleeding in acute upper GI bleed?
Platelet count below 50,000/mm3 requires platelet support
If on anticoagulants, give FFP and vitamin k
Serum calcium may drop after blood units given, replace with calcium gluconate
Tranexamic acid may be helpful
How does biliary obstruction present?
Jaundice RUQ pain and tenderness Fever Itching Dark urine and pale stools Septic shock
What investigations are indicated in biliary obstruction, and what may they show?
Wcc- increased U+es- renal failure LFTs- increased bilirubin, alp, ggt, and amylase if concomitant pancreatitis Blood cultures CRP USS - dilates ducts and gallstones AXR- aerobilia may be due to gas forming organism ERCP- stones in CBD MRCP
What may cause biliary obstruction?
Gallstones Malignancy Postoperative stricture Primary sclerosing cholangitis Primary biliary cirrhosis
How is biliary obstruction managed?
Analgesia
Antibiotics if septic
If dilated ducts:
Indicates gallstones
ERCP to decompress biliary system
If not dilated ducts:
Autoantibodies- pANCA, AMA
When stable, consider ERCP, liver biopsy
What is a differential for ascites?
Ovarian cyst
Obesity
Pregnancy
Abdominal mass
What are causes of ascites?
Cirrhosis and portal hypertension Malignancy Congestive cardiac failure Pancreatic ascites Nephrotic syndrome Hypothyroidism Infection eg TB
What investigations are indicated in ascites?
U+es, glucose, FBC, pregnancy test, LFTs, blood cultures, amylase
Ascitic tap unless malignant cause!
USS, axr, ct scan?
Urine sodium, 24hr protein
After treating the cause, how is ascites treated?
Restrict salt intake to 90mmol a day
Paracentese- if tense or moderate. Replace albumin afterwards
Start spironolactone at 100mg a day
How can AKI be defined?
Abrupt (within 48 hours) reduction in kidney function
Absolute increase in serum creatinine of >/= 26mmol
Or
>50% relative increase inn serum creatinine
Or
Reduction in urine output - less than 0.5 ml/kg per hour for more than six hours
How does AKI present?
Asymptomatic Incidental finding on biochemical screening Oliguria Malaise, confusion, seizures, coma Nausea, anorexia, vomiting Haematuria Vasculitic rash Multi organ failure
What are pre renal causes of AKI?
Hypovolaemia Hypotension Renal artery emboli Renal artery stenosis and ACEI Hepatorenal syndrome
What are post renal causes of AKI
Renal vein thrombosis Increased intrabdominal pressure HIV drugs Ureteric stones Prostatic hyper trophy
What are renal causes of AKI?
Vasculitis eg SLE Glomerulonephritis Acute tubular necrosis- due to ischaemia, septicaemia, gentamicin, radio contrast, malaria Scleroderma crisis Calcium/urate oxalate overload
What investigations are indicated in AKI?
UandEs FBC- anaemia suggests chronic RF Coagulation- to detect DIC, SLE LFTs- hepatitis, paracetamol OD Blood cultures Immunology- antigens etc CRP - raised in Vasculitis Protein strip- for para proteins, BJ proteins Urine dipstick, Micro and culture Renal USS CXR to assess heart size, pulmonary oedema ECG - hyperkalaemia
How is AKI managed?
Treat hyperkalaemia- calcium gluconate, glucose and insulin, salbutamol nebs, dialysis?
Treat metabolic acidosis- 50-100ml of 8.4% bicarbonate via central line
Treat pulmonary oedema
Oxygen, CPAP?, IV GTN, IV furosemide, Diamorphine
Assess hydration and fluid balance- if depleted, fluid challenge with saline
Treat infection
Stop nephrotoxic drugs
Identify intrinsic renal disease
Relieve obstruction
What are common causes of acute confusion?
Pain or discomfort- urinary retention, constipation
Hypoxia
Infection- systemic/localised
Metabolic disorders- renal failure, liver failure, acidosis, hypercalcaemia
Endocrine disease- thyrotoxicosis,
Addison’s disease, DM
Cardiac- MI, CCF, endocarditis
Neuro- head injury, subdural haematoma, cns infection
Drugs- benzodiazepines, opiates, digoxin, cimetidine, steroids, anticholinergics, recreational
Alcohol/drug withdrawal
What are the initial symptoms of acute alcohol withdrawal?
Peaking at 12-30hr, subside by 48hr: Anxiety Tremor Hyperactivity Sweating Nausea and retching Tachycardia Hypertension
Tonic clonic seizures may occur later
What are features of delirium tremens?
Coarse tremor, agitation, delusions, hallucinations
Fever, sweating, tachycardia
Rarely lactic acidosis, ketoacidosis
Hypoglycaemia, wernicke korsakoff psychosis
How is acute alcohol withdrawal managed?
Rehydrate, monitor urine output and blood glucose
IV pabrinex 8 hourly five days or thiamine 100mg PO bd for a week
Chlordiazepoxide
What is the triad of wernickes disease?
Opthalmoplegia- nystagmus, VI nerve palsy
Ataxia
Confusion state
Diagnosed by reduced red cell transketolase activity
Can DKA occur in patients with type 2 diabetes?
DKA predominantly occurs in insulin dependent diabetes. It does not usually occur in non insulin dependent diabetes, but is increasingly being seen in type 2 diabetics, particularly of afrocaribbean origin
What are the clinical features of DKA?
Polyuria Polydipsia Weight loss Weakness SOB with kussmauls (sighing) breathing Abdominal pain Vomiting Confusion and coma
What may precipitate DKA?
Infections
Non compliance with treatment
Newly diagnosed diabetes
What investigations are indicated in DKA?
Blood glucose - may not be high! ABG U+Es Urinalysis - ketones FBC - increased WBC Urine and blood cultures Plasma ketones CXR to investigate infection Amylase- may be high in absence of pancreatitis, although pancreatitis may occur in DKA
Ketoacidosis requires positive urinary or plasma ketones and ph <= 7.30
What is the management if DKA?
Consider HDU/ICU, central line, arterial line, urinary catheter if sever acidosis, hypotension, oliguric
Insulin- 50u soluble insulin in 50ml NaCl at rate of 6-7units/hr
Fluids- 500 saline over 15-30mins until SBP is greater than 100. Then 1l two hourly for six hours and 1l three hourly for nine hours
Potassium replacement in second bag of fluid
Monitor blood glucose, capillary ketones and urine output hourly
Potassium replacement and glucose replacement when potassium and glucose drop
What is the presentation of HONK?
Usually previously unknown diabetes in an elderly patient
Severe dehydration
Impaired consciousness
Respiration is usually normal
Patient is at risk of venous and arterial thromboses and may present with stroke, seizures or MI
What may precipitate HONK?
Infection MI or CVA GI bleed Poor compliance with oral anti diabetic agents Diuretics, beta blockers, antihistamines
Investigations in honk?
High glucose U+es show dehydration- hypernatraemia ABG - relatively normal compared to DKA FBC - polycythaemia or leucocytosis ECG- mi or ischaemia CXR - look for signs of infection Urinalysis and mc&s
How is honk managed?
Insulin infusion at 2-4u per hour. When blood glucose reaches 15mmol/l, commence 5% glucose infusion
IV fluid- 1l saline over first hour, the. 1l two hourly for 4 hrs,
Potassium replacement
Treat underlying cause
Thromboprophulaxis!
How does hypoglycaemic coma present? Hint: more than just coma
Sympathetic overactivity (glucose <2.6) Confusion Slurred speech Focal neurological defect Coma
What investigations should be made in hypoglycaemic coma?
Blood glucose- for obvious reasons
U&Es - hypoglycaemia is more common in diabetic nephropathy
Take blood prior to glucose administration
What are causes of hypoglycaemia?
Insulin
Sulphonylurea
Alcohol
Salicylates
Hypopituitarism Acute liver failure Adrenal failure Myxoedema Sepsis Malaria
How is hypoglycaemic coma treated?
If patient conscious and cooperative- oral glucose 50-100ml, or 3 glucose tablets
If reduced level of consciousness- 50ml of 50% glucose IV, or 1mg glucagon IM if no venous access
What factors comprise the wells score for DVT assessment?
Active cancer (including treatment up to six months previously)
Paralysis/immobilisation of leg
Recently bedridden for >3 days or major surgery within four weeks
Localised tenderness along distribution of deep venous system
Entire limb swollen
Calf swelling >3cm relative to other leg
Pitting oedema
Dilated collateral superficial veins
Subtract two points if:
Alternative diagnosis at least as likely as DVT
What investigations should be taken in DVT?
Venous compression ultrasonography- usually 90% accurate
D-dimers- to exclude PE
Consider coagulation screen, screen for malignancy eg ultrasound/ct abdomen and pelvis
Which patients should be anticoagulated with DVT? Based on wells score
Wells >/=1: performed dimer:
If negative, exclude DVT
If positive, perform USS - if positive, treat as DVT
Wells >/=2: perform d dimer and USS
If USS positive, treat
If d dimer positive but USS negative repeat USS in one week
What anticoagulants are used in DVT management?
LMWH- once daily SC injection
Warfarin- always use LMWH first!
Anticoagulated for three months
Consider thrombolysis for recurrent extensive, proximal thromboses
What are the symptoms of PE?
Sudden onset pleuritic chest pain
Breathlessness
Haemoptysis
Postural dizziness or syncope
Massive PE may present as cardiac arrest
What are the signs of PE?
Tachycardia Tachypnoea Cyanosis (large PE) Pleural rub or effusion Thrombophlebitis in lower limbs Mild fever may be present
Signs of raised right heart pressures and cor pulmonale- raised jvp, tricuspid regurgitation, paras thermal heave
What investigations are indicated in PE?
ABG - may show low O2 and low CO2 due to tachpnoea
ECG - sinus tachycardia and non specific ST and T wave changes. Cor pulmonale - RAD and RBBB
CXR- may be normal- this is suggestive of PE if respiratory compromise!
Blood tests - neutrophil leucocytosis
D dimer
VQ or CTPA
What is the management of PE?
Cardiac monitor, pulse, BP, resp rate, O2 sats
High flow oxygen
Venous access and start IV fluids
LMWH for all patients with High or intermediate risk of PE until diagnosis confirmed
NSAIDs for analgesia
If positive diagnosis:
Anticoagulate with warfarin- target INR 2-3 for four weeks at least
What are the presentations of paracetamol overdose, and when do these occur after ingestion?
Within 24 hours
- generally asymptomatic- possibly nausea, vomiting, anorexia,
24-36 hours
Hepatic necrosis- jaundice, RUQ pain, vomiting? Confusion
Over 72 hours
Encephalopathy, renal failure, lactic acidosis
What are some complications of paracetamol overdose
Acute liver failure- GI bleeds, hypoglycaemic , cerebral oedema
Pancreatitis
Lactic acidosis
Acute tubular necrosis- renal failure
What investigations should be done in paracetamol overdose?
Paracetamol - at four hours! UandEs- renal failure FBC - thrombocytopenia Glucose LFTs Prothrombin ABG lactic acidosis
What is the management of paracetamol overdose?
Activated charcoal 50g or gastric lavage if presents within one hour
Treat with NAC if 4h paracetamol places above treatment line on graph
First infusion over 15min, second over 4h, third over 16h
If allergic, give methionine
If high risk lower threshold for treating with NAC- high risk if: phenytoin, carbamazepine, rifampicin, high alcohol, anorexic or AIDS
If present before 8 hours - paracetamol levels before acetylcysteine
If present after 8 hours - give acetylcysteine straight away
What is a differential for cardiogenic shock?
MI Aortic dissection Arrhythmia Valvular disease Overdose of cardiac depressant Myocarditis
What is a differential for anaphylactic shock?
Recent drug therapy
Food allergy
Insect stings
What is a differential for Hypovolaemia shock?
GI haemorrhage Aortic dissection AAA rupture Fluid losses- diarrhoea, vomiting, burns Third spacing Adrenal failure
What is a differential for distributive shock?
Sepsis Liver failure Drug overdose- calcium antagonists Adrenal failure Neurogenic shock
What is a differential for obstructive shock?
Cardiac tamponade
Pulmonary embolus
Tension pneumothorax
Within what timeframe must broad spectrum antibiotics be administered in septic shock?
Within one hour
What are signs of anaphylaxis?
Skin redness Urticaria Conjunctival injection Angiooedema Rhinitis Laryngeal obstruction- choking, cough, stridor Bronchospasm Tachycardia Hypotension
What is the immediate management of anaphylaxis?
Maintain airway- consider intubation or emergency cricothyroidotomy if necessary
Give 100% oxygen
Give IM adrenaline 0.5-1mg- or IV if venous access
Establish venous access if not - fluid bolus/challenge
Give Hydrocortisone 200mg, chlorphenamine 10mg
How may Hyponatraemia present?
Mild Hyponatraemia is usually asymptomatic
Severe Hyponatraemia presents with disturbed mental state, restlessness, confusion, irritability, seizures and coma
What investigations are necessary in Hyponatraemia
Serum osmolarity
Urinary sodium
Assessment of patients volume assessment
What are causes of Hyponatraemia in hypovolaemic patients?
Renal losses (High urinary sodium)
Diuretics
Addison’s
Nephropathy
Non renal losses ( low urinary sodium)
GI losses- N+V
Burns
Fluid sequestration- peritonitis, pancreatitis
What are causes of normovolaemic Hyponatraemia?
Syndrome of inappropriate anti diuretic hormone - due to trauma, malignancy, Vasculitis, infection, lung disease
SIADH also caused by opiates, haloperidol, amitriptyline, cyclophosphamide, thiazides, vincristine
What is SIADH?
Excessive ADH secretion- ADH increases water absorbed in the kidneys
This results in high urine osmolarity and low serum osmolarity
How is Hyponatraemia typically managed?
Exclude pseudohyponatraemia- calculate osmolar gap
If volume depleted start IV normal saline. Do not correct by more than 10mmol in first 24 hrs
If SIADH, restrict fluid intake to 750ml per ???
How does subarachnoid haemorrhage typically present?
Sudden and severe thunderclap headache, radiating from the occiput with associated neck stiffness
Often occurs on bending/lifting heavy objects
Time to peak onset is usually less than a few seconds
Nausea, vomiting, dizziness
Reduces gcs
Seizures are uncommon but may occur
Herald bleed- unusually severe headache days or weeks before main bleed
Within what timeframe should a patient with suspected SAH be scanned?
Within 24h- 95% correct
When is Lumbar puncture indicated in SAH investigation?
Not usually required
Consider when ct scan is normal but history is highly suggestive
Xanthochromia if positive
What is the immediate management of SAH?
Protect airway, give oxygen
Treat seizures with drugs
Correct hypotension if necessary- nifedipine if diagnosis established to reduce vasospasm
ECG monitoring and treat dysrhythmias
Venepuncture for clotting screen and UandEs (Hyponatraemia from SIADH)
Arrange urgent cr head and lp if necessary
Analgesia
Regular neurological observations
Refer to neurologists for clipping/coil
What is status epilepticus?
Continuous tonic clonic convulsions lasting 30mins or longer, or convulsions so frequents that each attack begins before the previous convulsion ends
What are causes of status epilepticus?
Cerebral tumour Hypoglycaemia Head injury Low sodium, calcium, or magnesium Drug overdose Drug/alcohol withdrawal Hypoxia eg post cardiac arrest Anti epileptic non compliance
What is the management of status epilepticus
Open the airway
Give oxygen
Take blood for UandEs, glucose, calcium, magnesium, LFTs, FBC, toxicology if required
Anti epileptic therapy
Lorazepam
Diazepam as alternative to lorazepam
Start infusion if phenytoin - req ECG monitoring
If seizures continue, give phenobarbitol
If lasts greater than 60 mins, transfer to intensive care
What conditions may mimic a stroke?
Cerebral tumour- if presents over days
Brain abscess- pyrexial
Focal migraine
Subdural haematoma- variable consciousness
Post seizure (todds paresis)- although seizures occur in 5-10 percent of strokes
Hypoglycaemic attack
Encephalitis
When should patients suspected of stroke have a CT head?
All patients suspected of stroke should be scanned within 24h to detect if haemorrhagic stroke
Urgent CT if: Depressed level of consciousness History of anticoagulant treatment No available history Features suggestive of- SAH, SDH, space occupying lesion, cerebral infection Indications for thrombolysis
What are the indications for thrombolysis in acute stroke? And when should it be administered?
Give 300mg aspirin
IV alteplase, within three hours of onset of symptoms
Patient must have measurable neurological deficit
BP must be maintained below 180/105
Exclude if: MI, stroke, head trauma within three months LP within seven days Major operation within 14 days Previous GI, intracranial bleed
How does a total anterior (carotid) circulation infarct present?
Contralateral hemiplegia and hemianaesthesia in two contiguous areas (face, upper/lower limb)
Homonymous hemianopia
Higher cerebral dysfunction:
If left sided- global dysphasia
If right sided- unilateral neglect of contralateral space
How does a partial anterior (carotid) circulation infarct present?
Usually present with two out of the three components of the TACI subtype
How does lacunar infarction present?
Infarcts in small penetrating vessels- often due to hypertension
Pure motor or sensory stroke
Ataxic hemiparesis
How does posterior cerebral artery infarction present?
Contralateral homonymous hemianopia (or quadrantinopia)
Mild contralateral hemiparesis/hemisensory loss
Dyslexia
Memory impairment
What scoring system assesses risk of stroke following a TIA?
ABCD2
Age- >60 BP- >140/90 Clinical features- unilateral weakness or speech disturbance Duration of symptoms- >60mins Diabetes
What investigation can be done to confirm vascular territory/pathology in Suspected TIA
MRI
Ct if MRI contraindicated
How does opiate overdose present?
Pinpoint pupils
Resp depression and cyanosis
Possibly low BP
Hypotonia
How is opiate overdose managed?
Monitor RR (and depth), O2 sats, ECG for arrhythmias
Give oxygen
IV access
UandEs, CPK
Any comatose/respiratory signs requires CXR for infection, emboli, non cardiogenic pulmonary oedema
Naloxone, given IV in blouses until patient is rousable and resp depression corrected
Start infusion to avoid resedation!
What are complications of opiate overdose?
Non cardiogenic pulmonary oedema- may require CPAP or mechanical ventilation
Rhabdomyolysis may occur in opiate induced coma
IV drug users may develop right sided endocarditis and septic pulmonary emboli
Paracetamol containing preparations, such as codydramol, may cause renal or hepatic failure
How does tricyclic antidepressant overdose present?
Anticholinergics features such as dry mouth, dilated pupils, blurred vision, sinus tachycardia, urinary retention, myoclonic jerking and hallucinations may occur
Cardiac arrhythmias and coma may occur later
What are other complications of TCA overdose?
Severe toxicity - coma with respiratory depression, hypoxia, metabolic acidosis
Neurological signs of toxicity include loss of oculocephalic and oculo vestibular reflexes, ophthalmoplegia.
Hypothermia, skin blistering, rhabdomyolysis are also reported
What is the management of TCA antidepressant?
If CNS depression, monitor in ICU/HDU
Lavage/charcoal if within one hour
ECG should be recorded to asses arrhythmia/qrs prolongation
Resp failure may require intubation and ventilation
Alkalinization with boluses of bicarbonate if long qrs, metabolic acidosis, hypotension, or arrhythmias
Treat hypotension with glucagon or vasopressors, and fluid resus
Tricyclic coma may last 24-48hr, and require sedation
What is the management of AF in haemodynamically unstable patients?
Hypotensive patients- external defibrillation using synchronised shock, unless chronic AF
If DC shock fails:
IV amiodarone
Correct hypokalaemia
Attempt further dc shock
How should AF be managed in haemodynamically stable patients?
Rate control, and then rhythm control if appropriate
AF > 2 days duration: Control rate with - digoxin/b-blocker/verapamil/diltiazem/amiodarone Start LMWH Restore SR with amiodarone Consider DC cardioversion
AF <2 days duration:
Attempt chemical cardioversion: flecainide, amiodarone
If cardioversion unsuccessful, consider rate control as for AF greater than 2 days
How does aortic dissection present?
Chest pain- abrupt onset severe, anterior chest pain most commonly radiating to the inter scapular region. Usually tearing in nature and most severe at its onset
Sudden death or shock- due to aortic rupture or cardiac tamponade
Congestive cardiac failure- due to aortic incompetence
Patients may present with signs of occlusion of the branches of the aorta- renal failure, stroke, acute limb ischaemia, mi
What signs may be found in examination in aortic dissection?
May be normal
Usually hypertensive on presentation- but may be hypotensive
Aortic valve regurgitation
Neurological deficits due to carotid artery dissection or compression or spinal artery occlusion
What investigations are indicated in aortic dissection?
ECG- may be normal or non specific
CXR- may be normal, or show wide mediastinum, aortic knuckle enlargement
Bloods- FBC, UandEs, cardiac enzymes, crossmatch
Echocardiography - esp transoesophageal- first line!
MRI angiography - gold standard!
Spiral ct with contrast
What is the immediate management of aortic dissection?
Resus/ITU Cannulas FBC, UandEs, crossmatch Arterial line Morphine Correct BP
Ascending aorta (type a)- surgical repair and BP control
Descending aorta (type b)- medical management with aggressive BP control
How does pericarditis present?
Central chest pain, also pleuritic, relieved by sitting forward
May be SOB
Other symptoms may reflect underlying disease- fever, cough, arthralgia, rash, faintness
Venous pressure rises if effusion develops. Look for signs of cardiac tamponade
What are causes of acute pericarditis?
Idiopathic Infection- viral, bacterial, TB Dressers syndrome Malignancy- breast, bronchus, lymphoma Uraemia SLE, RA, wegeners, sarcoidosis Hypothyroidism Trauma Radiotherapy Hydralazine, procainamide, isoniazid
What investigations are indicated in acute pericarditis?
ECG- saddle shaped ST segment, some t wave inversion, PR segment depression
Usually all leads involved
Echocardiography- may demonstrate pericardial collection
Enables assessment of LV function
FBC, UandEs, CRP, cardiac enzymes, CXR
Where appropriate- viral titres, blood cultures, autoantibodies, TFTs, diagnostic pericardial tap
Acute pericarditis management?
Consider admission
Analgesia- NSAIDs
Steroids- if pain does not settle- prednisolone
Colchicine
Pericardiocentesis- if serious or signs of tamponade
Antibiotics if infection suspected
How does acute pancreatitis present?
Abdominal pain- epigastric or generalised, of rapid onset, dull constant and boring. May radiate to the back it between the scapular, may be relieved by leaning forward.
Nausea and vomiting
Peritonitis with epigastric tenderness
Localised rebound tenderness or general abdominal rigidity. No BS
Grey turners (flank) or cullens (umbilical)
What investigations should be ordered in acute pancreatitis?
Amylase FBC- leucocytosis UandEs- urea may be raised Glucose- may be raised LFTs- AST and bilirubin raised Hypocalcaemia CRP- elevated ABGs- hypoxia and metabolic acidosis AXR CXR - pleural effusion USS - gallstones Ct abdomen- pancreatic necrosis
What is the management of acute pancreatitis?
IV access
Fluid replacement if necessary
Oxygen if necessary
Keep NBM
Monitor blood glucose and treat with insulin if needs be
Pethidine- causes least sphincter of oddi spasm
Octreotide- suppresses pancreatic enzymes
Liaise with surgeons
Antibiotic prophylaxis with cefuroxime
After head injury, which risk factors suggest that ct head should be performed within one hour?
Any one of:
GCS <15 at two hours after injury on assessment
Suspected open or depressed skull fracture
Signs of basal skull fracture
Post traumatic seizure
Focal neurological deficit
More than one episode of vomiting since head injury
What clinical features are part of the wells DVT scoring system?
Active cancer- treatment ongoing or within six months
Paralysis, paresis or recent plaster immobilisation of legs
Recently bedridden for three days or more or major surgery within 12 weeks
Entire leg is swollen
Calf swelling by more than three cm compared with asymptomatic leg (measured 10cm below ischial tuberosity)
Putting oedema of symptomatic leg
Collateral superficial veins
Previously documented DVT
One point for each, subtract two points for equally likely alternative diagnosis, greater than two points indicates high risk of DVT
When is an ankle X-ray indicated according to the Ottawa ankle rules?
Only if pain in the malleolar zone and any one of:
Bone tenderness at posterior edge or tip of lateral malleolus
Bone tenderness at posterior edge or tip of medial malleolus
Inability to weight bear both immediately and in casualty department
What are the components of the trauma triad of death? And what is it’s significance?
Hypothermia
Acidosis
Coagulopathy
Seen in patients who have sustained severe traumatic injuries, and results in a significant rise in the mortality rate
What factors may cause coagulopathy in a trauma patient?
Hypothermia
Massive transfusion
Or both
