Finals Medicine Surgery Flashcards
Managing hyper kalmia
10ml 10% calcium chloride/gluconate over 5-10 min Insulin/glucose infusion Salbutamol Calcium resinous Identify and manage underlying cause
Hyperkalemia on ECG
4 features
Tall tented T wave
QRS a complex broaden
PR prolonged
P wave flattened
Wolf Parkinson white syndrome
Delta wave (characteristic slurred up slope)
(Pre-excited AF sometimes)
PR short
(Accessory pathway: bundle of Kent)
ECG changes of ACS (chronological)
Normal Peaked T wave ST segment elevation Q wave formation and loss of R wave (anterior chest leads) T wave inversion
4 criteria for STEMI/Emergency re perfusion
2 mm ST elevation in 2 or more contiguous chest leads
1 mm ST elevation in 2 or more limb leads of same territory
New LBBB or LBBB in clinical MI
True posterior MI
RV hypertrophy on ECG
R axis deviation
Dominant R wave in lead V1
Inverted T waves spreading from right side of the heart
Axis deviation
Look at I and avF
If away from each other then L axis deviation
If towards each other then R axis deviation if both positive then normal
IE bacteria
Strep
Staph
HACEK
The HACEK organisms are a group of fastidious Gram-negative bacteria that are an unusual cause infective endocarditis (IE), which is an inflammation of the heart due to bacterial infection.[1] HACEK is an abbreviation of the initials of the genera of this group of bacteria: Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella corrodens, Kingella.[1] The HACEK organisms are a normal part of the human flora, living in the oral-pharyngeal region.[2]
Causes of dominant R wave in V1/V2
Posterior MI
PE
RBBB
RVH
DUchenne muscular dystrophy
Dectrocardia
WPW
Why is it important to diagnose posterior MI?
Posterior MI can cause back pressure and raise JVP.
Usually when we see JVP elevation, we tend to give diuretics because we think it’s R heart failure. However diuretics can be fatal for posterior MI as we’re decreasing the preload, ie stretching… (Sterling law)
Mesenteric ischemia (classic triad)
GI emptying
Abdo pain
Underlying cardiac disease
JVP waves
http://youtu.be/cLETr8qmXPQ
How to differentiate a jugular venous pulse from the carotid pulse
JVP: Not palpable. Obliterated by pressure. Characterised by a double waveform. Variable with respiration - it decreases with inspiration. Enhanced by the hepatojugular reflux
Waveforms of JVP
Waves[2][3][4]
a - presystolic; produced by right atrial contraction.
c - bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase).
v - occurs in late systole; increased blood in the right atrium from venous return.
Descents
x - a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole.
y - the tricuspid valve opens and blood flows into the right ventricle.
The a and v waves can be identified by timing the double waveform with the opposite carotid pulse. The a wave will occur just before the pulse and the v wave occurs towards the end of the pulse. Distinguishing the c wave, x and y descents is an almost impossible task.
Causes of raised jugular venous pressure
Heart failure.
Constrictive pericarditis (JVP increases on inspiration - called Kussmaul’s sign).
Cardiac tamponade.
Fluid overload, eg renal disease.
Superior vena cava obstruction (no pulsation).
Abnormalities of jugular venous pressure
Abnormalities of the a wave: disappears in atrial fibrillation.
Large a waves occur in any cause of right ventricular hypertrophy (pulmonary hypertension and pulmonary stenosis) and tricuspid stenosis.
Extra large a waves (called cannon waves) in complete heart block and ventricular tachycardia.
Prominent v waves
Tricuspid regurgitation - called cv or v waves and occurring at the same time as systole (a combination of v wave and loss of x descent); there may be earlobe movement.
Slow y descent
Tricuspid stenosis.
Right atrial myxoma.
Steep y descent Right ventricular failure. Constrictive pericarditis. Tricuspid regurgitation. (The last two conditions have a rapid rise and fall of the JVP - called Friedreich's sign.)
Austin-flint murmur
soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.(in similar way to MS)
AR signs
large-volume, ‘collapsing’ pulse also known as: Watson’s water hammer pulse
Corrigan’s pulse (rapid upstroke and collapse of the carotid artery pulse)
low diastolic and increased pulse pressure
de Musset’s sign (head nodding in time with the heart beat)
Quincke’s sign (pulsation of the capillary bed in the nail; named for Heinrich Quincke)
Traube’s sign (a ‘pistol shot’ systolic sound heard over the femoral artery; named for Ludwig Traube)
Duroziez’s sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethoscope)
Drugs not to be used in severe AS
Nitrates (risk of syncope)
TAVI
Transcatheter aortic valve implantation
AF definition
Uncoordinated and disordered contraction of atria at fast rate which leads to initiation of ventricular contraction through the AV node at varying intervals… Thus leading to an irregularly irregular pulse
NY Heart Association classification of HF
I Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
II Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m).
Comfortable only at rest.
IV Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
What sign is pathognomic of HF?
3rd heart sound
Most common causes of HF in UK
CAD
HTN
Alcohol
Valvular disease
Lifestyle modifications in HF?
Smoking
Alcohol
Salt intake
Limit fluid intake (<2L)
TTT of HF
ACEI/ARB
Betablockers
Spironolactone/eplerenone
Diuretics for fluid overload but don’t impact prognosis
Other ttt for HF
Revascularisation if CAD
Bi ventricular pacemaker /defibrillator if dysynchrony
Transplantation
LVAD
Symptoms of IE
Lethargy
Fever
Night sweats
Less common:
New heart failure
Embolic phenomena (stroke)
IE on examination
New murmur
Splenomegaly
Embolic phenomena (splinter hges, osler’s nodes, janeway lesions, petechiae
Evidence of aetiology: IVDA, infected cannula, recent surgery
Ix in IE
3 blood cultures (different sites / different times) Echo (find vegetation) Baseline blood test (CRP) ECG Urine (hematuria)
Transoesophageal Echo (TOE) vs TTE in IE
TTE (60% sensitive) vs TOE (90% sensitive)
Dx of IE
Modified Duke criteria
2 major
1 major + 3 minor
5 minor
Major criteria:
1) evidence of endocardial involvement with either vegetarians/abscess on echo or new murmur
2) typical microorganism from 2 separate blood cultures
Minor criteria
1) predisposition (cardiac lesion/IVDU/line)
2) fever (>38)
3) vascular phenomena (arterial emboli)
4) immunological phenomena (glomerulonephritis)
5) echo abnormalities but no vegetation/abscess
Surgical replacement of infected valve in IE: when?
Evidence of HF (caused by infected valve, abscess or collection)
Heart block (caused by infection with virulent organisms unlikely to be cleared with antibiotics)
Large vegetation at risk of embolisation
Prosthetic valve endocarditis (always almost requires surgical Mx)
Prognosis of IE
Mortality 20%
Worse prognosis:
prosthetic valve
Embolic phenomena
Staph aureus
Causes of MR
Acute MR:
from papillary muscule rupture or dysfct following MIA, perforation or valve leaflet during IE
Chronic MR:
Causes: Rh fever, mitral heart disease prolapse. Functional MR in HF
Examination findings of MR
Pansystolic murmur
?third heart sound
Apex beat displaced
Basal creps + peripheral edema (HF)
MS finding on ECG
Bifid P wave = P mitrale
Due to LA enlargement
Surgical Mx of MS
PBMV: percutaneous balloon mitral valvotomy
Mitral valve repair
Mitral valve replacement
Causes of TR
Rh heart disease
Endocarditis (mainly IVDA)
Carcinoid heart disease
Most common: Dilation of RV (usually due to L heart failure, PHTN or RV infarct)
Carcinoid heart disease
Carcinoid heart disease is common in patients with carcinoid syndrome, and occurs in up to 50% of these patients.iiiIt is characterised by right sided cardiac involvement, caused by plaque-like deposits of fibrous tissue which are thought to be caused by serotonin, via action on the 5HT2b receptoriv.These deposits are most commonly seen on valve cusps and leaflets, but can be anywhere in the cardiac chambers, and even in the pulmonary arteries or aorta. The left side of the heart is relatively protected, with the pulmonary circulation filtering out the majority of the serotonin produced by the tumour. Overt left sided disease has been described in patients with a patent foramen ovale, bronchial carcinoid and patients with very high levels of serotonin
Signs in TR
Pansystolic murmur at L sternal edge
Prominent systolic wave in JVP
Pulsatile hepatomegaly (pathognomic)
Carcinoid syndrome
Carcinoid tumour in GI tract or bronchi that secrete 5-HT.
5-HT leads to flushing wheezing and diarrhea
Cardiac causes of syncope
HAPE HOCM AS PE Atrial Myxoma
AF
Heart block
Patients who don’t get classical chest pain
Elderly
DM
Atypical presentation of MI (in DM and elderly)
SOB
Syncope
Sweating
N&V
Complications of MI
FAM
Failure
Arrhythmias (commonest VT/VF… DC cardioversion)
Murmur (MR or VSD)
Approach to systolic murmurs
Chest pain…?
Chest pain + palpitations…?
Dizziness + chest pain…?
Chest pain…? AS
Chest pain + palpitations…? Mitral
Dizziness + chest pain…? AS
Symptoms of AS
Syncope
Angina
Dyspnea
Stenosis vs Sclerosis
Sclerosis:
No radiation
Normal pulse
Normal in elderly
Causes of malar flush
MS Pregnancy SLE Parvovirus Any hyperdynamic state (thyrotoxicosis)
Graham steel murmur
Leakage of pulmonary valve… Pulmonary regurgitation… Early diastolic murmur
Increased JVP a
R sided heart failure TR/TS SVC obstruction Heart block CCF
When JVP elevated, how to differentiate between TR/TS and SVC obstruction
SVC obstruction is non pulsatile while TR/TS is
VSD murmur
Usually asymptomatic in finals
Very loud pansystolic murmur throughout precordium + thrill
Murmur louder at sternal edge compared to apex
Machinery like murmur
Signs of previous CABG in exams
Midline sternotomy scar
LIMA
Legs (saphenous)
Arms (radial artery)
Prosthetic valve signs
Median sternotomy scar (no leg scar)
Bruised skin (on warfarin)
Audible clicks from end of bed
Prosthetic first heart sound
Complications of prosthetic valve
Failure (valve dehiscence) Infection Bleeding Anaemia (from anticoagulant, hemolytic anemia, secondary to IE) Theomboembolic
CHA2DS2VASC
C Congestive heart failure (or Left ventricular systolic dysfunction) 1
H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1
A2 Age ≥75 years 2
D Diabetes Mellitus 1
S2 Prior Stroke or TIA or thromboembolism 2
V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1
A Age 65–74 years 1
Sc Sex category (i.e. female sex) 1
Electrolytes disturbance causingbTdP
Hypokalemia
Hypomagnesemia
Bifascicular block
RBBB + LAD
Trifascicular block
RBBB + LAD + 1st degree heat block
WPW
AVRT (1% mortality vs 0% mortality in AVNRT)
Definition of MI
Detection of rise or fall of cardiac biomarker (trop) + at least 1 of the following:
- symptoms of ischemia
- ST changes or new LBBB
- pathological q waves
- imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Cardiac sounding chest pain
- constricting discomfort in front of chest, neck shoulders jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN within about 5 min
DD of chest pain
MS chest pain Pneumonic/pleuritic chest pain Pericarditic chest pain GORD/Gastric/Upper abdo Aortic dissection/AAA
STEMI Definition & Management
Def:
- ST elevation > 2 mm in anterior leads in 2 consecutive leads
- or ST elevation 1 mm in 2 consecutive limb leads,
- or new onset of LBBB
Mx:
- PAMI and CP<12h or pt still complaining of CP
- far from PAMI then thrombolysis (streptokinase, alteplase, tinctplase)
Post-reperfusion:
- beta blockers
- DAPT (dual antiplatelet therapy) 12 months
- Statin high intensity
- ACEI/ARB
Mx of NSTEMI
MONAC (initially) Assess risk (GRACE score for risk of death/MIA) Start beta blockers, anti-coagulation, high intensity statin, ACEI/ARB
Definition of HF
Abnormality of cardiac structure and or function leading to failure of the heart to deliver xylem at a rate equivalent to the requirement of the metabolising tissues.
Clinically, typical symptoms are (SOB, swelling and oedema, fatigue) and signs (raised JVP, pulmonary crackles) resulting from abnormality of cardiac structure / fct
HF types
- HFREF vs HFPEF (reduced vs preserved ejection fraction)
- Acute vs chronic
- left vs right
- severity (NYHA grade I to IV)
Causes of HF
- Myocardial disease: CAD, cardiomyopathy
- Valvular heart disease
- Pericardial disease
- Endocardial disease
- Arrhythmia
- conduction disorder
- high output status / volume overload / congenital HD
Pathophysiology of HF
Pathological re-modelling of the ventricle with dilation and impaired contractility
Signs of HF
SOB exertion Raised JVP Pulse abnormalities (irregular/ tachycardia) Murmur S3 gallop Displaced apex Pulmonary creps Hepatomegaly Oedema Ascites
Digoxin ttt effects on ECG
Reduced wave amplitude
ST segment depression
Increased u wave amplitude
Shortened QT interval
Pleural tap Ix
Protein
Glucose
LDH
Cell count, culture and microscopy cytology
AAFB and culture if suspecting TB
Ligth’s criteria
Used when protein 25-35g/l or patients with abnormal serum protein
Transudate < 30g/L
Exudate > 30 g/L
Simultaneous measurement of pleural fluid and serum
- pleural fluid protein/serum protein > 0.5
- pleural fluid LDH/serum LDH>0.6
- pleural fluid LDH>2/3 upper limit of normal
Any criteria met… Effusion=exudate
Causes of transudates
CCF Cirrhosis Hypoalbuminemia Nephrotic syndrome Hypothyroidism
Causes of exudate
Infection (pneumonia) Empyema (pleural pH of <7.2 is highly suspicious) TB Neoplastic RA Trauma Sarcoidosis Pancreatitis Esophageal rupture
CAP: typical and atypical bacteria
Typical: Strep pneumoniae H influenzae S aureus G- organisms
Atypical: Mycoplasma pneumoniae Legionella Pneumophilia Chlamydia pneumoniae/psittaci
CURB 65
Confusion +1
Blood Urea Nitrogen (BUN) > 19 mg/dL (> 7 mmol/L) +1
Respiratory Rate ≥ 30 +1
Systolic BP < 90 mmHg or Diastolic BP ≤ 60 mmHg +1
Age ≥ 65 +1
0-1: Treat as an outpatient
2-3: Consider a short stay in hospital or watch very closely as an outpatient
4-5: Requires hospitalization with consideration as to whether they need to be in the intensive care unit
HAP causative organisms
G- Enterobacteria
S Aureus
Klebsiella
Risk factors for aspiration pneumonia
Reduced GCS
Neurological conditions: stroke , bulbar palsies, MG, drug alcohol misuse
Signs of CF
Underweight Cyanotic Finger clubbing Coarse crackles throughout both lung fields Wheeze
Mx of CF
MDT approach Dietitian (malnutrition) Physio (postural drainage) Pancreatic enzymes supplements IV/nebulised antibiotics Bronchodilators Inhaled recombinant DNAase (improve FEV1) Lung transplant
Causes of bronchioecstasis
Genetic (CF, Karatgener’s, primary ciliary dyskinesia)
Post-infective (pneumonia, TB)
Post childhood infection (measles, pertussis)
Bronchial obstruction (foreign body, tumour)
Hypogammaglobulinemia
Allergic bronchopulmonary aspergillosis
AI disorders (RA)
Risk factors for PE
Recent surgery (hip/knee, pelvic/abdo) Recent lower limb fracture Malignancy Recent hospitalisation Previous Hx of VTE Pregnancy Prolonged immobility Long-haul travel OCP
Signs of PE
Breathlessness Pleuritic chest pain Cough Haemoptysis Clinical evidence of DVT Tachypnea Tachycardia Raised JVP Hypotension Raised JVP Pleural rub on auscultation
ECG pattern in PE
Tachycardia
Right heart strain/RBBB
S1Q3T3 (large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III)
Definition of sarcoidosis
Multi-system disorder characterised by non-caseating granulomas. Aetiology unknown
Sarcoidosis: Respiratory signs and symptoms
Breathlessness Chest pain Malaise / reduced exercise tolerance Cough - usually dry Low grade Pyrexia Bilateral hilar lymphadenopathy on CXR Lung fibrosis
Sarcoidosis: non pulmonary manifestation
Erythema nodosum Lymphadenopathy Hypercalcemia Hepatosplenomegaly Lupus pernio Posterior or anterior uveitis Keratoconjunctivitis sicca Enlargement of parotid glands Neurosarcoidosis Cardiomyopathy/Arrhythmia Arthralgia
Causes of interstitial lung disease
Idiopathic pulmonary fibrosis Hypersensitivity pneumonitis Sarcoidosis Pulmonary eosinophilia Coal workers pneumoconiosis Malignancy Previous infection Cryptogenic organising pneumonia Langerhans cell histiocytosis Drugs (amiodarone, cyclophosphamide, bleomycin)
Treatment of Idiopathic pulmonary fibrosis
Triple therapy: steroids + azathioprine + n-acetylcysteine
Lung transplant
Hypersensitivity pneumonitis
= extrinsic allergic alveolitis
Farmer’s lung most common
Horner’s syndrome
Ptosis
Miosis
Anhydrosis
Caused by Pancoast tumour
SVC obstruction s&s
Facial suffusion
Upper limb swelling
Distended jugular veins
Para neoplasticism drone
PTH-RP: hypercalcemia (SCC)
SiADH: hyponatremia
Eaton-Lambert syndrome (Lambert-Eaton myasthenic syndrome (LEMS) is a disorder of neuromuscular transmission caused by impaired presynaptic release of acetylcholine).
Ectopic ACTH production - Cushing (SCLC)
TB extrapulmonary manifestations
CNS: meningeal TB Genitourinary TB Bone TB (Potts disease) Skin TB (lupus vulgaris) Peritoneal TB Pericarditis (active or constrictive) GI TB
TB Ix
Sputum samples (AAFB smear and culture) Early morning krone for AAFB if renal disease suspected CXR Mantoux Bronchial washing or biopsy
TB Drug side effects
Rifampicin: liver function, urine orange
Isoniazid: peripheral neuropathy (give pyridoxine)
Ethambutol: retrobullar neuritis
Pyrazinamide: abnormal liver enzymes
Wegener granulomatosis TTT
Steroids
Cyclophosphamide
Infliximab
Aspergillosis six
Serum precipitins
Acute exacerbation of asthma: Mx
Oxygen Nebs Salbutamol 5 mg Nebs Ipratropium 0.5 mg IV hydrocortisone 200 mg Back to back Nebs Theophylline (check they're not already on it) Magnesium (1.2-2g IV)
If treating a patient that looks like acute exacerbation of asthma… And after giving all treatment no improvements, what can it be?
Pneumothorax (do Xray): asthmatic at higher risk of developing pneumothorax
Super added Infection
S&s in PE not usually asked
Syncope
PE
Coma due to resp failure
Cardiac arrest
Na and K daily requirements:
Na 100mmol/24h (1.5-2 mmol /kg/24h)
K 60 mmol/24h (1 mmol/kg/24h)
Fever and fluid requirement
Give 1 extra litre of fluid saline per degree rise every 24h
Adequate urine output
0.5 ml/kg/h
Wells score for PE diagnosis
clinically suspected DVT — 3.0 points
alternative diagnosis is less likely than PE — 3.0 points
tachycardia (heart rate > 100) — 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
history of DVT or PE — 1.5 points
hemoptysis — 1.0 points
malignancy (with treatment within 6 months) or palliative — 1.0 points
Traditional interpretation[9][10][15]
Score >6.0 — High (probability 59% based on pooled data[16])
Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data[16])
Score 4 — PE likely. Consider diagnostic imaging.
Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.
BTS pre-test probability score for PE
Pt has clinical features compatible with PE: raised RR, hemoptysis, pleuritic chest pain
Plus 2 other factors:
1- absence of another reasonable clinical explanation
2- presence of a major risk factor
If 1 and 2 high probability
If 1 or 2: intermediate probability
If none: low probability
In what circumstances do u use thrombolysis in PE?
In Massive PE with cardiac instability
Signs of PE
Tachycardia Tachypnea RV strain / pulmonary hypertension - high JVP - RV heave - loud P2 - TR Systemic hypotension (SBP<100) Cyanosis
On ECG: - Sinus tachy (commonest) - R sided strain - AF/atrial flutter/atrial tachycardia - RAD - partial or complete RBBB - TWI anteriorly +- laterally +- inferiority - S1Q3T3 - ST depression - P pulomonale - ST elevation (V1-V3) 1 reported case ECG can be completely normal
JVP anatomical position
The Jugular Venous Pressure (JVP) is found between the sternal and clavicular heads of the Sternoclavicular Muscle (SCM); usually just above the clavicle.
Coronary arteries and MI
RCA infarct:
- inferior MI (leads II, III and aVF)
- posterior MI (prominent R wave in V1/V2)
LAD infarct:
- anteroseptal (V1/V2)
- anterior (V3/V4)
- anterolateral (I, aVL, V3-6)
- excessive anterior (I, aVL, V1-6)
Circumflex infarct:
- lateral (I, aVL, V5-6)
- isolated posterior (prominent R wave in V1-2)
ST elevation in aVR?
Left stem occlusion (very dangerous)… ST elevation probably in All leads then
How is a fluid challenge done?
250 ml bolus of colloid administered as quickly as possible. Response in CVP or urine output should be seen within min. (Importance of size and duration of CVP response rather than the actual values recorded)
Shock: definition and types
Abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation (ie cardiac output is unable to meet the tissues metabolic requirements)
Hypovolemic (most common: hemorrhagic shock after injury)
Septic
Cardiogenic (from blunt injury, tamponade, air embolus, infarct).
Anaphylactic
Neurogenic (spinal injury causes shock because of loss of sympathetic tone (presenting as hypotension and bradycardia) which may compound and present hypovolemia)
Addisonian (withdrawal from steroids)
Quantifying Hypovolemic Shock
Class I: 0-15% blood loss (750ml)
Class II: 15-30% blood loss (750-1500ml)
Class III: 30-40% blood loss (1.5-2l)
Class IVA: >40% >2l
BP starts falling at >30%
Hypernatremia and urine osmolality
If urine osmolality is high: hyponatremia due to dehydration
If urine osmolality is low: diabetes insipidus
Causes of cardiogenic pulmonary oedema
Remember acronym HAVM
1- hypertension
2- arrhythmia
3- valve disease (aortic/mitral)
4- MI/IHD
5- failure of prosthetic heart valve 6- cardiomyopathy 7- VSD 8- negatively inotropic drugs 9- pericardial disease
T wave morphology
Normal
Inverted (new old MI)
Biphasic (ischemia)
Tented peak (in hyperkalemia, hyperacute in ischemia)
VT vs SVT (with aberrancy)
More likely VT if Concordance Very wide qrs > 150 msec Captured beats Fusion beats
LVH on ECG
S1R6 > 35 mm
RVH on ECG
Prominent R V1 > 10 mm
Shock definition
Inadequate tissue perfusion and oxygenation
Definition/Dx of cardiac arrest
2 things
- unresponsive
- no major pulse
Diagnosis of tamponade clinically
Beck’s triad: low arterial blood pressure, distended neck veins, and distant, muffled heart sounds
Causes of PEA (pulseless electrical activity)
These possible causes are remembered as the 6 Hs and the 6 Ts
Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hyperkalemia or Hypokalemia Hypoglycemia Hypothermia Tablets or Toxins (Drug overdose) Cardiac Tamponade Tension pneumothorax Thrombosis (Myocardial infarction)(Pulmonary embolism) Tachycardia Trauma (Hypovolemia from blood loss)
Signs of cerebellar disease
DANISH T
- Dysdiadochokinesis - impairement of rapid alternating movements
- Ataxia-broad based gait, falling to side of lesion
- Nystagmus - horizontal nystagmus with fast beat towards side of lesion
- Intention tremor (finger to nose and heel to shin testing)
- Stoccato speech-usually with bilateral lesions (cerebellar dysarthria)
- hypotonia
- titubation (rhythmic tremor of head)
Causes of cerebellar disease
Demyelination (MS)
Space-occupying lesion in posterior fossa
Brainstem vascular disease
Infection - HIV abscesses
Toxicity (alcohol, anticonvulants, CO, lead)
Inherited (friedrich’s ataxia, sca (spinocerebellar ataxias)
Degenerative
Charcot-Marie tooth disease (peroneal muscular dystrophy)
Distal limb weakness : pes cavus Wasting of small muscles (hands, arms...) Hyporeflexia Absent ankle jerks High stepping gait
Azathioprine: what test before starting?
Test TPMT
Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine …
Adrenaline dose for cardiac arrest
1 mg IV
1/10000 concentration
Speed of anaphylactic reactions
Food reaction=Resp arrest in 30-35 min
Insect stings: shock 15 min
IV meds: within 5 min
Anaphylaxis : adrenaline dose?
0.5 mg IM
1/1000
Mix of UMN and LMN degeneration symptoms and no sensory abnormalities…?
Think Motor neurone disease
Heart failure – Chest X ray signs
ABCDE
Heart failure – Chest X ray signs
ABCDE
Alveolar oedema (bat’s wings) kerley B lines (interstitial oedema) Cardiomegaly Dilated prominent upper lobe vessels Effusion (pleural)
Causes of blackout
CRASH
Cardiac (stokes Adams)
Reflexes (vagal overactivity, postural hypotension)
Arterial (migraine, Tia, shock…)
Systemic (glucose drop, resp(hypoxia), blood (anemia)
Head (epilepsy…)
Chorea (definition and causes)
Non rhythmic purposeless jerky flitting movements Causes Huntington Sydenhan Wilson L-dopa
Sparing of forehead wrinkling and blink
Frontales and orbicularis muscle have bilateral UMN representation
(LMN lesion: the final common pathway is destroyed)
Drug induced SLE
CHIMP Carabamazepube Hydralazine Isoniazidr Minocycline Procaibamide, pyrazinamide
Causes of fractured neck of femur
Osteoporosis
Trauma
Combination
What to know in Hx of fractured neck of femur
Age
Comorbidity
Preinjury mobility
Social hx
Describing a fracture radiograph
Location: (which bone and part) Pieces: simple/multifragmentory Pattern: transverse/oblique/spiral Displaced/undisplaced Transverse/angulated
Red flag for bone pain
Malignancy
Infection
severity pain
Hx to ask about in OA
Pain (exertional, rest, night)
Disability (walking distance /stairs…)
Deformity
Previous history (trauma and infection)
Treatment given (physio injection operation)
Other joints affected
Problem as a child (development dysplasia of the hip)
OA management
Conservative : analgesics, physio, walking aids, avoidance of exacerbating activity, injections (steroid, viscosupplementation)
Operative : 1- replace (knee/hip) 2- realign (knee/big toe) 3- excise (toe) 4- fuse (big toe) 5- synovectomy (rheumatoid) 6- denervate (wrist)
Most common causes of large bowel obstruction
Cancer
Diverticular disease
Volvulus
Bird’s beak sign on barium swallow
Achalasia
Fourth heart sound
Long standing aortic stenosis or hypertension
Third heart sound
Heart failure: rapid ventricular filing
Signs of chronic liver disease
- General: cachexia, icterus, excoriation, bruising
- Hands: leuconychia, clubbing, dupuytren, Palmar erythema
- Face: xanthelasma, parotid swelling, fetor hepaticus
- Chest and abdomen: spider naevi, caput medusa, reduced body hair, gynecomastia, testicular atrophy
Signs of hepatomegaly
palpation and percussion:
- mass in r upper quadrant, moves with respiration, not able to get above, dull to percussion
- estimate size: finger breaths below diaphragm
- Smooth our craggy/nodular (malignancy cirrhosis)
- Pulsatile (TR in CCF)
Auscultation
- Bruit over liver (hepatocellular carcinoma)
Evidence of an underlying cause of hepatomegaly
Tattoos and needle marks Pigmentation Cachexia Midline sternotomy scar Infectious hepatitis / alcohol Haemochromatosis Malignancy CCF
Evidence of DECOMPENSATED chronic liver disease
AAA
Ascites (shifting dullness)
Asterixis (liver flap)
Altered consciousness (encephalopathy)
Causes of hepatomegaly
- Big 3
Cirrhosis (alcoholic)
Carcinoma (secondaries)
CCF - Other
Infectious (hep b c)
Immune (pbc, psc, autoimmune hepatitis)
Infiltrative (amyloid and myeloproliferative disorders)
What do patients with portal hypertension die of
Variceal bleeding which would be a medical emergency
What it’s major hemorrhage protocol
Hh
Urobilinogen in obstruction
Is negative (we all have a tiny amount)
What happen to bile salts in obstruction
They leak into bloodstream
What are true liver enzymes
Albumin
Bilirubin
Alkaline phosphatase
ALT (alanine amino transferase)
In addition need to measure AST and GGT
What does polio do
Old polio which damages the nucleus of the lower motor neuron
Mixed upper and lower motor neurone disease
ALS
Child pugh score
Classification score for cirrhosis
Based on
Bilirubin Albumin INR Ascites Encephalopathy
Felty’s syndrome
is characterized by the combination of rheumatoid arthritis, splenomegaly and neutropenia.
Causes of unilateral kidney engagement
Polycystic kidney disease
Renal Cell carcinoma
Simple cysts
Hydronephrosis (due to ureteric obstruction)
Causes of bilateral kidney enlargement
Polycystic kidney disease Bilateral renal Cell carcinoma Bilateral Hydronephrosis Tuberous sclerosis Amyloidosis
Evidence of immunosuppressive
Ciclosporin: gum hypertrophy and hypertension
Steroids: cushingoid appearance, thin skin ecchymoses…
Top 3 causes for renal transplantation
Glomerulonephritis
Diabetic nephropathy
Polycystic Kidney disease
Top 3 causes for liver transplantation
Cirrhosis
Acute hepatic failure (hepatitis a b, paracetamol overdose)
Hepatic malignancy
Causes of gum hypertrophy
Drugs: ciclosporin, phenytoin, nifedipine Scurvy Aml Pregnancy Familial
Dorsal columns
Vibration
Proprioception
Spinothalamic tract
Pain
Temperature
Tabes dorsalis
Tabes dorsalis, also known as syphilitic myelopathy, is a slow degeneration (specifically, demyelination) of the nerves primarily in the dorsal columns (posterior columns) of the spinal cord (the portion closest to the back of the body). They help maintain a person’s sense of position (proprioception), vibration, and discriminative touch.
Horner’s syndrome causes
Causes of Horner syndrome may also be classified as involving first-order, second-order, or third-order neuron lesions.
First-order neuron lesions that may give rise to the syndrome include the following:
Arnold-Chiari malformation
Basal meningitis (eg, syphilis)
Basal skull tumors
Cerebral vascular accident (CVA)/Wallenberg syndrome (lateral medullary syndrome)
Demyelinating disease (eg, multiple sclerosis)
Lesions in the hypothalamus or medulla
Intrapontine hemorrhage
Neck trauma (eg, traumatic dislocation of cervical vertebrae or traumatic dissection of the vertebral artery) - Horner syndrome occurring in association with spinal cord trauma suggests a high cervical cord lesion because it does not occur with lesions below T2 or T3
Pituitary tumor
Syringomyelia
Second-order neuron lesions that may give rise to Horner syndrome include the following:
Pancoast tumor (tumor in the apex of the lung, most commonly squamous cell carcinoma)
Birth trauma with injury to lower brachial plexus[6]
Cervical rib
Aneurysm or dissection of the aorta
Lesions of the subclavian or common carotid artery
Central venous catheterization
Trauma or surgical injury (eg, from radical neck dissection, thyroidectomy, carotid angiography, or coronary artery bypass grafting)[7]
Chest tubes
Lymphadenopathy (eg, Hodgkin disease, leukemia, tuberculosis, or mediastinal tumors)
Mandibular tooth abscess
Lesions of the middle ear (eg, acute otitis media)
Neuroblastoma[8]
Austin flint murmur
In cardiology, an Austin Flint murmur is a low-pitched rumbling heart murmur which is best heard at the cardiac apex.[1] It can be a mid-diastolic[2] or presystolic murmur[3] It is associated with severe aortic regurgitation, although the role of this sign in clinical practice has been questioned.[4]
Pericardiris on ECG
St elevation (,notchz,) Pr deression
Meeran eye slide
Micro aneurysm
Hard exudate
Blot hemorrhages
Background diabetic nephropathy
Patient needs good diabetic control: diet exercise maybe metformin (add gliclazide if needed)
Pros and cons ctpa vs vq scan
Ctpa: More radiation (not pregnant,) More available in hospitals Vq scan can be done only if xrays normal Ctpa can give more info (pleural effusion...) If pe wrong diagnosis
Commonest bacteria in teeth that might cause problems
Strep viridans
Pleurisy in paces
Pleural rub heard… Crunch… Walking on snow
Usually from: Primary infarction, or following pneumonia or following pulmonary embolus.
Horner syndrome
Horner syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner’s syndrome:
First-order neuron disorder: Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord).
Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor).
Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection).
Partial Horner’s syndrome In case of a third-neuron disorder, anhidrosis is limited to the middle part of the forehead or can be absent, resulting in a partial Horner’s syndrome.[3]
Eye out and down
Third nerve palsy
Surgical or medical
Look at pupil size
Surgery: posterior aneurysm…
In a squint
The outside image is from the weak eye
By doing cover test
Probably 6th nerve palsy or 3rd or complex ophtalmoplegia
Cause of complex opthalmoplegia
Graves disease (commonest)
MG
Retro-orbital tumour
Miller-Fisher syndrome (orbital guillain Barre syndrome) (one patient is usually in exams)
Eye slide Number 2
NOrmal fundus
What to see in background retinopathy
Hard exudates,(cholesterol)
Micraneyrysms,z(dots
Blot hemorrhages
Third slide eye Meeran
Cotton wool spots (used to be called soft exudates)
What are cotton wool spots
Retinal ischemia
Slide 4 Meeran eye
New vessels
Silver wiring
Diabetes
They present wiyh hyperosmolar… Weren’t diagnosed before
Slide 5 eye Meeran
Hdhdhd
Management of diabetic retinopathy
Background
Pre-proliferative: cotton wool spots. Suggests General ischemia. If left alone New vessels will grow. Needs Pan retinal phosphorylation
Proliferative: visible New vessels (this is an emergency weight be seen in exam)
Needs Pan retinal photocoagulation
Eye slide 6
See laser spots
Can ask if they have diabetes but might be shouted at
Pan retinal photocoagulation…
Older laser black burns
Newer lasers are paler
Pan retinal photocoagulation
Carefully avoid burning the macula
So we are sacrificing some peripheral vision tip maintain central vision
Eye slide 7
Retinitis pigmentosa
Retinitis pigmentosa
Retinitis pigmentosa (RP) is an inherited, degenerative eye disease that causes severe vision impairment and often blindness.[1] The progress of RP is not consistent. Some people will exhibit symptoms from infancy, others may not notice symptoms until later in life.[2] Generally, the later the onset, the more rapid is the deterioration in sight.[citation needed] Those who do not have RP have 90 degree peripheral vision, while some people who have RP have less than 90 degrees.
Retinitis pigmentosa with photonic acid
Chelsea and westminster site
Heritable
Many genetic syndromes example usher syndrome
(Deafness)
Refsum’s disease (failure to metabolize phytanic acid)
Can lead to blindness and would like to take Family history
Causes for hirner syndrome
Damage to sympathetic chain
Trauma to carotid sheeth (central line)
Apical lung tumour
Stages of hypertensive retinopathy
1- Silver wiring
2- av nipping
3- cotton wool and flame shaped hemorrhages
4- Papilloedema
Visits fields
Homonymous hemianopia (Cva (stroke), braintumour middle cerebral or occipital cortex)
Bitemporal hemianopia (pituitary tumour)
Unilateral hemianopia (Surgery): optic nerve… Check slide
Why right side perceived with left side brain
Check
How to present an acromegaly patient
Inspect hands… Check slide Meeran
Photos
Gtt with gh check igf1
Examine visual fields
How to present graves disease patient
How to tell if active or not
What investigations
Management
Check Meeran slide
Mechanism of lid lag
Sympathetic activation with high t3
Opposite of Horner
Eyelids don’t relax as quickly
Caused by adrenal activation
Cushing syndrome patient viva
If not on steroids
Active disease down by proximal myopathy, red Syria’s and thin skin
Investigations include urine free… Check slide
Rheumatology short case
Put hands on pillow and minimise discomfort
Subluxation (displacement without dislocation)
Mcp and pip joints
Is it active ) unlikely to be tender warm)
Any problems with adl (kettle button)
Proceed to viva
Ulnar derision of mcp joints
Swan neck deformity of fingers
Boutonniere deformity of the thumb
Management
Ix
DMard
Describe hands you see pic Meeran
Young patient
Pip involvement
Another case of ra
Had ra for 3 Months only… Needs biologics asap
Pip and mcp is ra
Urgent referral for specialist opinion
Needs pain control
Other oa
Dip Older patient No inflammation Wear and tear No autoimmune Aging of joint
Treatment is pain relief
No dmard
MENTION KNEES AND HIPS…
heberdens nodes
Care 4 hands Meeran pic
Describe
Thin shiny skin hard (sclerosis=hard)
Scleroderma
Autoimmune
Mixed connective tissue disease
Crest syndrome possible
Immunopharmacology therapy
Image 5 hands
Tophaceous gout
Management
Pain relief
Nsaid (just ndomethacin)
Aspirate joint
Negatively birefringent crystals
Acid uric metabolism
Ttt: indomethacin or colchicin
Interval glut: either xo inhibitor allopurinol or uricosuric =probenicid
Case 6: AS see pic
Vertebrae are ankylosed and fixed
Measure occiout to wall to decide how severe it is
Corrective Surgery to the back
Refer to specialist
Dermatology
Describe the skin lesions
Describe distribution: extensor area on less
Complications
Management
Describe Meeran first dermatology pic
Erythematous, scaly…well defined lesion
Onycholysis
If artritis, think of psoriatic arthropathy
Management of psoriasis
Moisturizer and creams
Cost tar… Check slide
Complications of fractures
- Local Nerve injuries (sensory motor autonomic conseQuences) LigameNts Local infection Compartment syndrome
Nonunion malunion causing deformity
Long term autonomic: reflex sympathetic dystrophy
General/systemic
Infection/sepsis uti
DVT PE
Shock hemorrhagic
Immediate Early late
Fractured NOF
Causes
Osteoporosis (older)
Trauma (younger)
Combination
In the context of c diff, what are pseudomembranes
Consist of neutrophils fibrin mucus and debris
Fractured nof history
Age
Comirbidity (Resp cardio diabetes cancer)
Pre injury mobility
Social history
Severe osteoarthritis
Wakes you up at night
Night pain in ortho
Osteoarthritis
malignancy
Infection
Slide on face and noise
Describe our:
This is oral candidiasis
Immunosuppressed, on steroids, bruising noise
On nose this is kaposi sarcoma
Erythema ab ignae
Erythema ab igne (EAI, also known as hot water bottle rash,[1] fire stains,[2] laptop thigh, granny’s tartan and toasted skin syndrome[2]) is a skin condition caused by long-term exposure to heat (infrared radiation).[3] Prolonged thermal radiation exposure to the skin can lead to the development of reticulated erythema, hyperpigmentation, scaling and telangiectasias in the affected area. Some people may complain of mild itchiness and a burning sensation, but often, unless a change in pigmentation is seen, it can go unnoticed.
Definition of Respiratory failure
Type 1 and 2
Po2 < 8
Type 1: only hypoxic
Type 2: hypoxic and hupercapnic
Complications of pseudomembranous colitis
Hypovolemic shock Electrolyte imbalance Hypoalbuminemia Perforation of bowel Toxic megacolon
Management of toxic megacolon
Subtotal colectomy
Appears as dilated colon with featureless wall on xray
What characterises neurogenic shock
Bradycardia Warm peripheries (pooling of blood)
Asa grading
American society of anesthesiologists grading system used to predict patient pre operative morbidity outside of Surgery type
1- normal healthy
2- mild systemic disease
3- severe systemic disease that limits activity
4- incapacitating systemic disease and life threatening
5- not expected to survive more than 24h
Features of portal hypertension
Ascites
Splenomegaly
Esophageal varies
Causes of foot drop
Common peroneal nerve lesion
Buerger disease
Vasculitis of medium sized vessels
Like intermittent claudication in young patients less than 45.
Gangrene…
Glasgow modified score to predict prognosis of pancreatitis
PANCREAS PO2 < 8 AGE > 55 NEUTROPHILS ACC > 15 CALCIUM < 2 RENAL (UREA) > 16 ENZYMES (LDH, AST) > 600 ALBUMIN < 32 SUGAR (GLUCOSE) > 10
Volkmann ischemic contracture
Complication of suprscondylar fracture
Due to brachial artery injury
Described add flexion contracture of hand and wrist caused by circulatory compromise and ischemia leading to fibrosis of forearm compartment.
Secondary to untreated compartment syndrome.
Brown sequard syndrome
Described features of unilateral transaction (hemisection) of the spinal cord.
Ipsilatetal loss of motor function with impaired joint posit ion and vibration sense (dorsal column dysfunction)
Contralateral sensory loss for pain and temperature.
Gastrochisis
Congenital defect in anterior abdominal wall next to umbilicus in newborn
Morton neuroma
Neuroma of the digital nerve of the foot that is most common between third and fourth metatarsals. Common cause of foot pain.
Frozen shoulder called
Adhesive capsulitis
Most common causes of small bowel obstruction
Adhesions
Hernias
Tumours
Most common causes of small bowel obstruction
Adhesions
Hernias
Tumours
Most common cause of large bowel obstruction
Tumour
Four cardinal symptoms of intestinal obstruction
Colicky abdominal pain
Distension
Vomiting
Obstipation (inability to pass fluids our feces)
Normal pressure hydrocephalus
Elderly commonly
Saturation of the ventricles without any signs of raised intracranial pressure
Triad of dementia, urinary incontinence and ataxia
What ate the vertebral levels of different organs in abdomen
Check…
Causes of high alkaline phosphatase
ALKPHOS any fracture Liver damage (posthepatic) Kancer Pagets disease of bone Pregnancy Hyperparathyroidism Osteomalacia Surgery
Peutz-Jeghers syndrome
Peutz-Jeghers syndrome, also known as hereditary intestinal polyposis syndrome, is an autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis).[1] Peutz–Jeghers syndrome has an incidence of approximately 1 in 25,000 to 300,000 births.[2]
Causes of clauducation
Spinal stenosis
Ambulatory blood pressure monitoring
Check cutoff for positive results
Causes of proteinuria and nephrotic syndrome
Glomerular Pathology:
- Minimal change
- Membranous
- Diabetes
- Amyloid
- SLE
Aneurysm: definition
This is the pathological localised permanent dilatation of an artery to more than 1.5 times its original diameter involving all 3 layers of its parent wall.PSEUDOANEURYSM DOESN’T INVOLVE ALL THREE LAYERS OF THE ARTERIAL WALL.
Causes of bowel obstruction
Small bowel obstruction is more common than large bowel. The most common causes of small bowel obstruction are - adhesions- hernias- cancersThe most common causes for large bowel obstruction are:- cancers- diverticular disease- volvulusThe causes of bowel obstruction can be divided into mechanical and non-mechanical causes.Mechanical causes can be classified according to their relation to the bowel wall:- luminal: gallstones, meconium, impacted faces, …- extramural: adhesions, cancers, hernia, volvulus- in the wall: congenital stenosis, strictures, IBD, diverticulitis, cancer…Non-mechanical causes, known as paralytic ileus, are due to - postop abdo surgery, - mesenteric ischemic- metabolic causes (hypokalemia, uremia, hypoglycemia and hypothyroidism)
Causes of clubbing
The most common cause of digital clubbing is idiopathic. However, there are many causes of clubbing and they can be classified into:- GI causes: IBD, PBC, coeliac- Resp causes: Lung Ca, bronchiecstasis (suppurating lung disease), CF, Mesothelioma, fibrosing alveolitis - cardiac causes: congenital cyanotic heart disease, endocarditis- other causes: familial, idiopathic, graves’ diseaseShamroth’s test
Ix for acute abdomen
!!! simple bedside tests:- ECG (to rule out ischemic/MI)- urinalysis (hematuria in renal calculi, UTI, or pregnancy test)- BM: blood sugar levels, if suspected DM presenting as abdo pain!!! Blood tests:— Simple tests- FBC (raised WCC in infection or anemia if GI bleed)- U&E: look for dehydration, renal failure, raised urea in case of acute GI bleed, electrolyte imbalance secondary to massive fluid shifts in pancreatitis or cases of bowel obstruction- LFT: for acute cholecystitis, or obstructive jaundice- Amylase: compulsory in acute abdomen. Raised in acute pancreatitis to at least greater than 3 times the upper limit of normal - G&S: if expecting an operation or if there is blood loss- Cross-match: if expect pt will need operation and will require blood transfusion (eg upper GI bleed taken to theatre)- ABG: if pt particularly sick, will help to gauge how sick he is. Lactate and pH are helpful indicators of level of shock and can help unmask conditions like mesenteric ischemia.— specialist tests (for pancreatitis for example: do BM, Ca levels, liver transaminases and CRP to score severity).!!! Imaging— plain films- erect CXR: if suspecting perforated intra-abdominal viscous…then looking for air under diaphragm. Film taken while patient sitting upright for at least 20 min prior to film taken, because air will need time to rise and demonstrate a pneumoperitomeum. Sign only present in 80% of cases- AXR: if bowel obstruction thought- Contrast films: gastrograffin enema if bowel obstruction or IVU for ureteric colic.— Ultrasound- USS liver: to scan biliary tree for evidence of gallstones or to measure size of common bile duct in suspected obstructive jaundice— CT scans:- CT KUB: first line Ix for renal calculi- CT abdo/pelvis: depends on the case but useful in pts not responding to ttt and in whom urgent Sx exploration is not mandated.
Question about discussing the management
Start with stating Hx, examination, Ix, differential diagnosis and ttt options.Ttt options can be either:- conservative: includes anything non-surgical. May be in the forms of IV fluids, NG tube for drainage of stomach contents and urinary catheterisation. Includes as well MDT approach (OT, PT, clinical nurse specialists) in chronic debilitating conditions such as OA or cancers- medical: any drugs (eg analgesia, antibiotics…). May also take form of more invasive but non-surgical ttt options, such as injection sclerotherapy in varicose veins or injecting Hemorrhoids. Some surgeons argue that endoscopic ttt options fall under this category.- surgical: any surgical procedure performed
Discussing surgical complications
2 main categories1- complications from anaesthetics: 1.1 damage to local structures (mouth, pharynx, teeth) 1.2 allergic reactions to agents (minor vs major) 1.3 slow recovery (due to poor cardiac, hepatic renal function…) 1.4 malignant hyperpyrexia (caused by anesthetic gas or suxamethonium) 1.5 awareness (pt paralysed but without effective anaesthetic)2. Complications due to surgery 2.1 related to any surgical operation: pain, infection, bleeding, DVt/PE 2.2 specific to the surgical procedure 2.2.1 immediate 2.2.2 early 2.2.3 late
Postop complications of total thyroidectomy
- Cpx from anaesthetics2. Cpx from surgery 2.1- general to any surgical operation 2.2- specific to thyroidectomy A- immediate (3 weeks): hypothyroidism, keloid scar formation, recurrence.FYI: primary hge or laryngeal edema compromising the airway is a surgical emergency. Surgical clips should be removed to facilitate evacuation and help relieve the immediate airway compromise (buys time before definitive surgical evacuation). Surgical clip removers always by the bedside of post-thyroidectomy pts.
Testicular pain age groups
- prepubertal: mumps orchitis, idiopathic scrotal oedema, testicular torsion- adolescent (10-21): testicular torsion (most likely), epididymo-orchitis, torsion of the Hydatid of Morgagni (7-14)- adult (>21): epididymo-orchitis (most likely), testicular torsion- all age groups: trauma
Focused Hx for Testicular pain
- patient age- testicular pain: bilateral (mumps orchitis), unilateral (testicular torsion or epididymo-orchitis), acute onset (torsion) vs gradual onset / hours (epididymo-orchitis), sharp pain (torsion) vs dull heavy (epididymo-orchitis), pain relieved by standing up or wearing scrotal support (epididymo-orchitis), radiation to thigh groin or abdomen (t10 dermatome) implies testicle, if to penile shaft or perineum implies idiopathic scrotal edema.- Urinary symptoms: dysuria, urinary frequency and urethral discharge commonly seen in epididymis-orchitis. Nothing in torsion.- sexual HX; relevant for epididymo-orchitis- swelling: + erythema = scrotal edema or mumps orchitis / just after trauma = hemToma / swelling can occur with torsion.- previous HX: torsion (usually intermittent torsion previously) - fever/vomiting: with epididymo-orchitis, torsion or mumps. Vomit from pain in torsion.
How to describe a scar
1- Identify scar: name with eponymous name or anatomically ((eg 2cm scar in R groin). Comment on whether scar recent (raised and pink/red) or old (flat and same colour as surrounding skin)2- check for incisional hernia: ask pt to cough or raise head off the bed3- suggest possible operations
Possible operations for Midline laparotomy scarWhat about Upper midline scar and lower midline scar
Exploratory laparotomyHemicolectomy Hartmann’sAAA repairUpper midline scar: splenectomy (massive)Lower midline scar: para-umbilical hernia repair, colectomy
Possible operations for Kocher’s or right subcostal scar
Open cholecystectomyPartial liver resectionAny biliary surgery
Reversed Kocher’s (left subcostal)
Open splenectomy
Possible operations for Double Kocher’s or rooftop scar (=R and L subcostal)
Ivor Lewis (Oesophagectomy)Complex pancreatic/gastric surgery
Possible operations for Mercedes scar or extended rooftop
Complex upper GI surgery (eg McKeown Oesophagectomy, gastrectomy, liver transplant
Possible operations for left nephrectomy scar or loin incision
NephrectomySpecialist renal surgery
Possible operations for Gridiron or McBurney’s scar
Appendicectomy
Possible operations for Pfannestiel scar
- pelvic surgery: bladder resection, prostatectomy, bilateral hernia repairs- gynae: C-section, cystectomy, hysterectomy
Possible operations for Rutherford Morrison or hockey stick scar
Renal transplant
(When seeing a renal transplant scar, what else would u like to examine/look for?
I would like to look for associated scars:eg - AV fistula at wrist, - median sternotomy scar, - CAPD (Tenckhoff) scar on abdominal wall or - infraclavicular scars from previous dialysis access (Vas Cath insertions)
Gridiron scar vs Lanz scar
Gridiron scar perpendicular to McBurney’s line at McBurney’s pointLanz is a transverse muscle splitting incision better for cosmetic result (incision follows Langers’s lines)
What structures would you go through in 1- an Appendicectomy scar?2- a midline laparotomy scar?
Appendicectomy scar: From superficial to deep:1- skin, subcutaneous tissue2- scarpa’s fascia, Linea alba3- muscle layers: external oblique, internal oblique than transfers us abdominis4- transversalis fascia5- extra peritoneal fat then parietal peritoneumMidline laparotomy scar: From superficial to deep:1- skin, subcutaneous tissue2- scarpa’s fascia, Linea alba3- transversalis fascia4- extra peritoneal fat then parietal peritoneum
What’s a peritoneum?
It’s a serous membrane that forms the lining of the abdominal cavity. It covers most of the intra-abdominal organs, and is composed of a layer of mesothelium supported by a thin layer of connective tissue. The peritoneum supports the abdo organs and serves as a conduit for their blood vessels, lymph vessels and nerves.
Pros and cons of midline laparotomy scar
Pros: - good access- can be easily extended- speed of closure and opening- relatively avascular (Linea alba)Cons:- incision more painful than transverse incision- scar crosses Langer’s lines (poor cosmetic appearance)- Narrow Linea alba below umbilicus (therefore can damage bladder)
What features determine the placement of laparoscopic ports?
In general, ports should be placed away from areas of high risk, such as:- previous scars, adhesions and known organomegaly- the vessels of the anterior abdominal wall should be avoided , particularly the inferior epigastric arteryThe minimum number of ports should be used (typically 3)The positioning of these ports should then allow for the target organ to be at an apex of an imaginary diamond formed by the various ports as well as the target organ itself.The 10 mm port is the camera and is useful for the removal of organs such as the gallbladder in a cholecystectomy. All other ports are typically 5mm in size.
Pros and cons of laparoscopic surgery
Pros:- shorter hospital stay and rehabilitation- less post-op pain- better cosmetic result- less wound complications- decreased handling of organs (eg bowel)- less trauma to tissues- later reduced incidence of postop adhesionsCons:- lack of tactile feedback to the operating surgeon- longer operation times- more technical expertise required, prolonged training- expensive equipment- difficulty in controlling massive bleed- increased risk of iatrogenic injury to surrounding organs- not always feasible due to CI (eg adhesions)
Nine regions of abdomen
From R to L:- Upper: R hypochondrial, Epigastric, L hypochondrial- Middle: R lumbar, umbilical, L lumbar- lower: R iliac fossa, suprapubic, L iliac fossa
Underlying organs behind the 9 abdominal regions
- R hypochondrial: liver, gallbladder, R kidney, hepatic flexure of colon- R lumbar: ascending colon, small bowel, R urinary tract- R iliac: caecum, appendix, terminal ileum, R ovary and R Fallopian tube- Epigastric: Liver (left lobe), pylorus, duodenum, transverse colon, head and body of the pancreas- Umbilical: Duodenum, small bowel, abdominal aorta- Suprapubic: Bladder, uterus- L hypochondrial: spleen, stomach, splenic flexure of colon, tail of the pancreas, L kidney- L lumbar: descending colon, small bowel- L iliac: sigmoid colon, L ovary and L Fallopian tube
Umbilical vs paraumbilical hernias
Central umbilical hernia-Clinical featuresOccurs following failed fusion of the anterior abdominal wall after birth.Often evident a few days after delivery.The hernias are usually small.The underlying defect is usually smaller than the visible hernia.A cough reflex is present. - Management:Most settle spontaneously and parents can be reassured.Surgeons are usually unhappy to operate before one year old.Strangulation never occurs in central hernias.Paraumbilical hernia- Clinical featuresOccur as a central swelling usually above or below the umbilicus.These hernias may become very large.More common in adults (especially women), than children.May be associated with obesity and weak abdominal muscles.The sac may contain both bowel and omentum.This is a true defect in the linea alba close to the umbilicus. - ManagementThese hernias will not resolve without surgical intervention.The patient should be advised to lose weight.Surgical repair is recommended because of strangulation risk.
Striae: causes and types
Due to rupture of the reticular dermisSilver striae: signifiant changes in weightBluish striae: present in hyoercortisolism
Abdominal signs in acute pancreatitis
Discolouration / bruising in haemoperitomeum, secondary to haemorrhagic pancreatitis or ruptured ectopic.Cullen’s sign: bluish discolouration around umbilicusGrey turner’s : bluish discolouration at the flanks
Interpretation of bowel sounds: absent, increased, tinkling
- Absent bowel sounds: paralytic ileus, peritonitis, obstruction, mesenteric ischemia/infarction- increased sounds: diarrhoea, obstruction- tinkling: ileus (disruptions caused by failure of peristalsis), a later phase of obstruction
Special tests for acute abdomen examination- McBurney’s point tenderness- Psoas sign- Obturator sign- rovsing’s sign- cough test- carnett’ sign- succussion splash- boas’ sign
- McBurney’s point tenderness: acute appendicitis. Found 1/3 of the way from ASIS to umbilicus- Psoas sign: hand above R knee and apply resistance and ask pt to flex hip. If this increases abdo pain, then positive sign for appendicitis.- Obturator sign: R knee flexed, and internal rotation of hip, if increased abdo pain, then positive sign for appendicitis.- rovsing’s sign: palpate in LIF. On releasing the pressure, if pt experiences pain in RIF, test positive for appendicitis.- cough test: pain experienced by pt when asked to cough in peritonitis, as this moves the peritoneum and causes pain when there is peritoneal irritation. This is another way to elicit rebound tenderness.- carnett’ sign: to differentiate abdo wall pathology (eg rectal sheath hematoma) vs pain caused by intra-abdo pathology. Ask pt to lift the head and shoulders off the couch or to straight leg raise both legs.- boas’ sign: pain that radiates from inflamed gallbladder in acute cholecystitis to the tip of R scapula. Leads to an area of skin just below scapula to become extremely sensitive to touch, resulting in pain (hyperesthesia)
What is the significance of palpating a tender gallbladder?
- this elicits Murphy’s sign, seen in cholecystitis. Pain on inspiration- if able to palpate a gallbladder, this is always pathological. If no coexisting jaundice, then this has resulted from obstruction of the cystic duct, resulting in mucocele or empyema- if co-existing jaundice, it implies obstruction of CBD and is thought to be caused by other causes besides gallstones. With gallstones, the gallbladder wall can become thickened and fibrosed after recurrent episodes of inflammation; but gallbladder enlargment typically arises as a result of carcinoma of the head of the pancreas, or another cause as stated in Courvoisier’s law
Courvoisier’s law
in the presence of an enlarged gallbladder which is nontender and accompanied with mild jaundice, the cause is unlikely to be gallstones.
Causes of abdominal ascites
Causes of ascites can be divided into those that can cause an exudate or a transudate exudate (>30g/l of protein)– peritoneal malignancy– infection (eg TB)– obstruction of IVC– obstruction of hepatic portal vein– acute pancreatitisTransudate (<30 g/l)– heart failure due to hydrostatic increase in venous return– cirrhosis of liver as a result of increased portal hypertension– hypoalbuminemia due to nephrotic syndrome
Key features to look for in hepatomegaly
- site: R hypochondrium: can extend into epigastrium if very large- palpation: can’t get above it- moves with respiration- not ballotable- dull to percussion- can be associated with splenomegaly
Key features for splenomegaly
- site: L hypochondrium- can’t get above it- moves down toward RIF with respiration- not ballotable- dull to percussion- palpable notch: enlarges towards the umbilicus/RIF
Key features in kiney organomegaly
- site: L or R flank (if very large, may involve the ipsilatera Hypochondria)- L1/L2 level- can get above it- moves vertically down on inspiration- ballotable- usually resonant due to overlying bowel- if bilateral, consider polycystic kidney disease
Causes of hepatomegaly
- jaundiced, smoothly enlarged: viral hepatitis, biliary tree obstruction, cholangitis- jaundiced, knobbly enlargment: malignancy (primary or secondary), cirrhosis, liver abscess, Hydatid cyst- no jaundice, smooth enlargment: CCF, cirrhosis, Budd-Chiari syndrome, amyloidosis - no jaundice, knobbly enlargment: primary hepatocellular Ca, cirrhosis
Causes of splenomegaly
- infection: malaria, EBV, CMV, TB- congestion: portal hypertension, CCF- infarction: subacute endocarditis- malignancy: leukaemia, lymphoma, myeloproliferative disorders- others: felty’ syndrome (RA, neutropenia, splenomegaly)
Causes of hepatosplenomegaly
- infection: infectious mononucleosis- cellular proliferation: polycythemia rubra Vera, myelofibrosis- malignancy: lymphoma, leukemia- others: amyloidosis, sarcoidosis, cirrhosis
What is portal hypertension
This is increased portal venous pressures to > 10 mm HgThe most common cause worldwide is post viral hepatitis, and in the UK it is alcoholic liver cirrhosis
What is Budd-Chiari syndrome
It’s a condition caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of- abdo pain- ascites- hepatomegaly
Causes of RIF mass
- skin and subcutaneous tissues, muscle: lipoma, sebaceous cyst, Psoas abscess, Psoas bursa- bowel: caecal carcinoma, crohn’s mass, TB mass, appendix abscess or mass- urological: transplanted kidney (common in exam), ectopic kidney, bladder carcinoma- reproductive system: males (ectopic testes, u descended testes) females (fibroids, ovarian tumours)- blood vessels: iliac artery aneurysms, lymphadenopathy, sachems varix, ruptured epigastric artery, femoral aneurysm.On L side, same + diverticular abscess or carcinoma of colon.
What are the indications for performing a DRE?
- acute abdomen assessment (appendicitis, peritonitis, lower abdo pain- prostate assessment: prostate hypertrophy or prostatic Ca- pre-procedure: before doing proctoscopy, sigmoidoscopy, colonoscopy- Dx purposes: constipation, change in bowel habit, anorectal pain or tenesmus…
What are haemorrhoids?How are they managed?
Surgical definition: Hemorrhoids are enlarged anal cushions (dilated veins)(Typical HX of painless bright red rectal bleeding… Can be painful if thrombosed)Management: conservatively: 1- sitz bath, analgesia and dietary advice2- injection sclerotherapy: Gabriel syringe containing 5% phenol in almond oil injected above the dentate line (beware not to inject in prostate gland and cause prostatitis)3- banding: rubber band placed around pile, which causes ischemia and shrinkageSurgical1- hemorrhoidectomy
What is dentate line (=pectinate line)?
It’s an anatomical landmark that divides the sensory part of the anal canal.Above it there is no sensation, but below there is, that’s why injection sclerotherapy is done above this lineThis line divides the upper 2/3 and lower 1/3 of the anal canal. Above it, we have columnar epithelium and below it’s stratified squamous epithelium.
Abdominal stoma examination
Do not remove the stoma bag in the examination unless you have been specifically directed to do so//Introduction//Inspection1- describe the site of stoma: LIF (colostomy) RIF (ileostomy) R lumbar (urostomy) (on the right because ureter is slightly shorter on R side), epigastric (gastrostomy/jejunostomy, or even loop colostomy), suprapubic (mucous fistula)2- estimate the size of lumen (large=colostomy/small=ileostomy or urostomy). Beware that if lumen is small, then this may have occurred from complications related to stomas, like stenosis or retraction. A prolapsed stoma will make the lumen look bigger.3- count number of lumens: single lumen (most cases: eg end stoma), double lumen (either looped or double stoma)4- examine for a spout: absence of spout (if lumen is flush with skin, it is probably a colostomy (unless prolapsed) vs spout present (ileostomies usually to keep irritant effluent off the skin. Urostomies as well).5- bag content: dark-green fluid and odourless (ileostomy), solid faeces and faeculent (colostomy), urine (urostomy)6- look for abdo scars: give a clue to what surgery they had (eg midline laparotomy scar in conjunction with colostomy, which can be from an abdominoperitoneal resection or Hartmann’s procedure)//Complete the examination: to complete my examination I would like to examine the perineum to look for the presence of a patent anal canal and anal stump (pouch left behind after colon is diverted surgically).Differentiation of a colostomy between AP resection (abdominoperineal) (in low-lying rectal Ca or severe UC) vs Hartmann’s (done as emergency for diverticulitis or bowel obstruction, secondary to colorectal Ca): Closed perineum vs patent anal canal.
Differentiation of a colostomy between AP and Hartmann’s
AP resection (abdominoperineal) (in low-lying rectal Ca or severe UC) Closed perineumHartmann’s (done as emergency for diverticulitis or bowel obstruction, secondary to colorectal Ca): patent anal canal.
What is a stoma
This is a surgically created connection between the GI or urinary tract and the skin. It can be temporary (reversible) or permanent.
How to distinguish between ileostomy and colostomy?
1- Site: RIFT (ileostomy) vs LIF (colostomy)2- Spout : present (ileostomy) vs Flush (colostomy)3- bag effluent: odourless dark-green liquid (ileostomy) vs solid faeces (colostomy)4- effluent volume: 500 ml (low output) to 1L (high output) (ileostomy)/ day vs 300 ml/day (colostomy)
What are the complications of a stoma?
These can be divided into general complications and complications specific to the stoma itself:- general cpx: nutritional disorders (eg vit b deficiency), renal stones, short gut syndrome, stoma diarrhea, psychological- specific complications: technical problems (such as ischemia, prolapse, parastomal hernia, stenosis or retraction). Practical problems (include malodour, skin irritation due to spillage of bag effluent).
Causes of abdominal pain?
Localisation of pain:- R hypochondrial: biliary colic, acute cholecystitis, ascending cholangitis, empyema, hepatitis, sub phrenic abscess- Epigastric: peptic ulcer disease, leaking AAA, acute pancreatitis, perforated duodenal ulcer- L hypochondrial: splenic infarct/rupture- R lumbar: renal and ureteric colic, pyelonephritis- Umbilical: leaking AAA, small bowel obstruction- L lumbar: renal and ureteric colic, pyelonephritis- R iliac fossa: appendicitis, ureteric colic, inguinal hernia, terminal ileitis, gynae pathology- suprapubic: distended bladder, large bowel obstruction, UTI, pelvic inflammatory disease- L iliac fossa: diverticulitis, ureteric colic, gynae pathology, inguinal hernia
How can pain be categorised?
Pain can be categorised depending on its aetiology:- visceral pain: diffuse pain that is poorly localised; usually described as being dull and aching in character—- foregut pain (described as being epigastric in site)—- mid-gut pain (usually felt in para-umbilical region)—- hindgut pain described as pain in lower abdo- parietal / somatic pain: well localised and sharp in nature, arising from peritoneal inflammation- referred pain: aching in nature and perceived as being near the surface of the body.
Indications for various types of stomas?
- feeding: jejunostomy, gastrostomy- decompression: caecostomy, gastrostomy- diversion: urostomy (ileal conduit), ileostomy (temporary or permanent), loop colostomy (currently performed using the sigmoid colon, 2 openings, 1 functioning to release stool and gas, 1 non-functioning), double-barrelled colostomy: both ends of the colon are brought to the surface next to each other and are sutured together along the anti-mesenteric border- exteriorisation: double barrelled colostomy, end colostomy (AP resection), end colostomy and rectal stump (Hartmann’s), end colostomy and mucous fistula
Typical structure of an orthopedic examination
LookFeelMoveSpecial testsNeurovascular examinationX-Rays
Phases of the gait cycle
1- Heel strike (heel touches the ground)2- stance phase (entire period where foot is on ground) (represents 60% of gait cycle)3- toe off4- swing phase (foot in the air for limb advancement)
Gait examination
////Look- check for walking aids or appliances (in presentation “this patient is walking unaided” or “the patient walks aided by a Zimmer fame”). Appliances include shoe raises, orthotics or calipers- ask for pt to walk: symmetry of arm swing, presence of pelvic tilt and stride length - carefully observe the gait: looking for 1- limp (gait smooth or halted (due to abductor weakness in Trendelenburg, or leg shortening or antalgic gait)) 2- distinctive pattern of the gait, 3- arm swing, 4- how the patient turns around////Special tests- Heel-to-shin pathology- Romberg’s test: if positive… Indicative of vestibular or proprioceptive problem
Patterns of gait
– antalgic gait: decreased stance phase and increased swing phase… Pathology=pain– Trendelenburg lurch: shoulders and trunk lurch sideways in order to bring the body weight over the affected limb. Pathology=weak abductors– drop foot: foot drops in swing phase, and the foot is lifted higher than normal so that the toes don’t drag along the ground. The foot may slap the ground prematurely. Pathology=peripheral neuropathy or injury to the nerves L5 supplying the ankle dorsidlexors (common peroneal or sciatic nerve palsy)– high stepping: compared to drop foot, both feet are raised here. Pathology=bilateral foot drop, proprioception or cerebellar disease– short leg: ipsilatera hip falls when pt weight bears on short leg. Pathology: congenital shortening, previous fracture– waddling: pt trunk moves from side to side with each step they take. Pathology=dislocation of hips, weakness of abductor muscles
What is antalgic gait?
It’s a gait with a decreased stance phase and increased swing phase, usually due to pain
What types of walking aids are there?
Walking aids can be broadly classified into sticks, crutches and frames.Various types in each group, eg Zimmer frame, elbow crutches, or a wooden stick with crook handles
Can u tell which side has the pathology from the position of the stick?
When using one stick, stick should be held in the opposite hand to the side of pathologyIf hip pathology, in opposite hand to reduce the weight bearing loadIf kmee pathology, usually held in ipsilateral hand
What is the Trendelenberg sign
Sign found in people with weak or paralysed abductors of the hip, namely gluteus medius and gluteus minimus
What to expect in examining a hip with osteoarthritis
!!! Look- Patient usually older than 50- Functional aids: walking aid, especially walking stick (held in the hands opposite to the affected hip)- Gait: obvious limp, angelic gait or Trendelenberg positive- From front: hip scar often seen in opposite hip (Patient often awaiting arthroplasty for the other hip), muscle wasting, leg length discrepancy- From the back: lumbar lordosis may be increased in those with fixed flexion deformity, scoliosis, scars from posterior approach!!! Closer inspection: affected leg will appear short, fixed flexion deformity!!! Feel: tenderness!!! Move: movements are generally restricted!!! Special tests: Thomas demonstrates a fixed flexion deformity
What does Trendelenberg test indicate?
Weakness of the hip abductorsMore specifically, - This could be a false positive, usually due to pain or poor balance on the patients part as a result of generalised weakness- Gluteal muscle inhibition due to pain from the hip joint- Gluteal muscle inefficiency due to congenital hip dislocation or coxa vara - Gluteal muscle paralysis from polio
How you investigate a patient with an osteoarthritic hip?
- simple blood tests such as renal function tests, because the patient is likely to be on long-term NSAID which may lead to interstitial nephritis- Specialist blood tests, particularly rheumatoid factor and ANA , to exclude a systemic cause- Imaging, which would include plain film radiographs of the affected hip with two views, AP and lateral, and views of the joint above and below
What radiological features to find in osteoarthritic hip?
Loss of joint spaceOsteophytesSclerosisSubchondral cysts
Radiological features of rheumatoid arthritis
Periarticular osteoporosisLoss of joint spaceMarginal erosionsAbsence of osteophytes
Management of osteoarthritis
MDT approach with input from orthopedic surgeon, gp, physiotherapist and occupational therapistDivided in:!!! Conservative measures:- Lifestyle changes ( Functional aids to help with daily living activities)- Walking stick held in the opposite hand- Weight loss and regular physiotherapy!!! Medical treatments involve:- Pain relief ( who analgesic ladder)!!! Surgical interventions- Vary according to age: if patient>50, total joint replacement is procedure of choice- For younger patients, they will have at least one revision in their lifetime, therefore benefit from other procedures such as repositioning osteotomy until an arthroplastybecomes a viable option
Features suggesting a total joint replacement be suitable
Intractable pain (with failure of conservative and Medical measures)Rest pain, instability or loss of mobility
What to find in hip affected by rheumatoid arthritis
- Patient has usually an established pattern of multiple joint involvement that is typically symmetrical- There is a marked Gluteal muscle and calf wasting- Affected limb is held in fixed fixation in external rotation- All movements are generally restricted and painful, whereas in osteoarthritis the movements may be restricted but often painless with a limited range
Hip examination… Main steps
//// Look- walking aids or appliances - observe from front: 1- level of hips and knees: symmetrical? 2- valgus/varus deformities of the knees 3- surgical scars 4- obvious leg length discrepancy?- observe from back : 1- surgical scars (don’t forget posterior approach to hip), 2- any gluten muscle wasting? 3- any scoliosis? (compensory scoliosis can be seen in true shortening)- examine gait- perform trendelenburg’s test//// closer inspection - measure leg length: apparent leg length (umbilicus to medial malleolus) and true leg length (ASIS to medial malleolus). If discrepancy do Galeazzi test//// Feel- palpate over bony landmarks for tenderness : (over ASIS, PSIS and greater trochanter for trochanter bursitis)//// Move- Thomas’ test: for fixed flexion deformity. And assess flexion (130o) extension (10o) at same time - check abduction (45o) and adduction (30o)- check rotation internal (35o) and external (45o)//// complete examination “ to complete my examination I would like to assess the neurovascular status of the lower limbs and examine the knees and back”- could ask for x-ray in 2 positions and for joint above and below
Pes cavus and pes planus
Pes cavus: arched feetPes planus: flat feet
Swelling in knee
- could be local effusion that may be reactive or secondary to osteoarthritis, haemarthrosis, (in tibial plateau fractures), septic arthritis (Dx with joint aspiration of the fluid and tested for MC&S and gram stain)- Prepatellar bursitis (housemaid’s knee), infrapatellar bursitis (clergyman’s knee- Popliteal fossa swellings (baker’s cyst)
What provides stability to the knee joint
The following ligaments:- ACL and PCL (intracapsular) stop the tibia moving anteriorly and posteriorly respectively in relation to the femur- Medial and collateral ligaments (extracapsular) provide support for the capsule of the knee.- Medial collateral attached to the medial tibial condyle and protects against a valgus force- Lateral collateral attached to the head of the fibula and protects against a varus force- Quadriceps and hamstrings are massive providers of stability to the knee joint
What is the purpose of the fibula
Acts as a support for the tibia, so in lower limb fractures if only the tibia is fractured it can be treated in plaster alone, as it is considered to be a relatively stable injuryWhen both tibia and fibula fractured, most centres treat with an intramedullary nail of the tibia, because this is classified as a unstable fracture
What to expect in examination of an osteoarthritic knee
!!! Look- Walking stick- Varus deformity, fixed flexion deformity- Opposite knee having a midline scar, indicating previous total knee replacement- Quadriceps muscle wasting- Antalgic gait !!! Feel- Joint line tenderness- Effusion may be present!!! Move- Crepitus on movement- Decreased range of flexion- Fixed flexion deformity of the knee may become apparent- Generalised tenderness on active and passive movement !!! Special tests- Positive McMurray’s test
What features would you look for in an X-ray of an osteoarthritic knee?
I would request a weight bearing X-ray of the knee, with AP and lateral views looking specifically for:- Loss of joint space- Osteophytes - sclerosis- Subchondral cysts Mnemonic LOSS
How would you manage osteoarthritis of the knee
Essentially managed in a similar fashion using an MDT management approach. Details specific to the knee include:- Physiotherapy to improve quadriceps muscle strength- Simple analgesia in the form of paracetamol or co-codamol - Walking aid in form of stick or framesIntra-articular steroid injection for temporary pain relief- Partial or total knee arthroplasty
How do you initially assess a Surgical Emergency?
It is important to state initially:”this is a surgical emergency. I will resuscitate the patient by:!!! Assessing the airways:- Give supplemental oxygen (high flow oxygen via a non rebreathable bag- Assess potency: 1)ask patient a question. If no answer, then 2) assess for evidence of airway compromise (anything blocking, blood vomits, suction using a Yankauer suction. Listen for stridor. 3) establish a patent airway by a) simple manoeuvres ( jaw thrust, chin lift, removing foreign bodies) b) airways adjuncts (oropharyngeal (guedel) or nasopharyngeal) c) secure or definitive airway (orotracheal intubation).!!! Checking the breathing- Monitoring: saturation probe or ABG - Inspection: cyanosis, check Respiratory rate, chest wall expansion, distended neck veins (pneumothorax), paradoxical chest wall movement (flail chest)- Palpation: tracheal deviation? Percussion for hyperresonance in pneumothorax or dullness in postoperative basal atelectasis or haemothorax.- Auscultate: !!! Assess circulation- Assess level of shock: cool? Clammy? Capillary refill time?- Monitoring: attach to monitor and check vital signs (HR, BP)- obtain IV access (2 large bore cannulae (grey or brown)- Resuscitation fluids: (crystalloids, colloids or blood)- Additional monitoring: urinary catheter, central line…!!! Assess disability- Neurological status: GCS, AVPU (alert, verbal response, response to pain, unresponsive)- Pupils: opiates (bilateral pinpoint pupils) or blown pupil (unilateral dilated pupil) in space occupying lesion (subdural or extradural hematoma)- BM glucose: !!! Assess environment/exposure- Exposure for bleeding..- Assess abdomen (pulsatile / expantile mass)!!! Reassess Always say that you will go back and reassess a b and c to check there is anything you have missed!!! Emergency investigations!!! Call for Senior help and advice!!! Definitive treatment (conservative, medical or surgical)Say that you will book an emergency theatre slot
What is a definitive airway:
Is one where a cuffed tube is secured in the trachea, ensuring patency
Atelectasis definition
Defined as the collapse or closure of the lung resulting I reduced or absent gas exchange. Alveoli are deflated. Acute onset may occur as a post operative complication or resultant of surfactant deficiency
What emergency investigations would you confident in a surgical patient?
- simple bedside tests: EGG, pregnancy test, BM glucose- Blood tests: FBC, U&E … ABG if critically ill- Imaging: erect chest X-ray, CT abdomen- Specialist investigations: depends on differentials (eg serum amylase in acute abdomen)- Exploratory laparotomy
How to manage a 35 year old woman complaining of right upper quadrant pain. Serum amylase is 3500.
This is acute pancreatitis.This is a surgical emergency1- initial resuscitation: I would resuscitate the patient, ensuring the patient’s airway is patent with access to high flow oxygen. I would then ensure the patient is breathing adequately. I will address the circulation by inserting 2 large bore cannulae whilst taking blood for pancreatic severity assessment at the same time. I would begin the patient on aggressive fluid resuscitation as thepatient is likely to have suffered significant third space loss.2- additional monitoring: to accurately guide fluid replacement I would like to assess the patient volume status through Clinical examination, the patient vital signs and urine output. Need for urinary catheter and a strict fluid balance chart documented in order to maintain positive balance3- call for help: at this point I would call for senior help and advice. After discussion with a senior colleague, I would like to consider the need for a central line to accurately guide fluid replacement4- assess severity: I would then like to assess the severity of this pancreatitis attack as this will help determine the level of Care the patient requires, particularly the need for an HDU bed. Using the modified Glasgow severity score, I would perform a arterial blood gas analysis on air to check for type over respiratory failure with pO2 less than 8 as this would suggest acute respiratory distress syndrome. I would also check for a Metabolic acidosis and serum lactate levels as this gives an indication of the level of shock. Other specific tests I would request include glucose levels to check for hyperglycemia as the patient may need an insulin sliding scale plus serum calcium levels and particularly a CRP as this helps to monitor and guide treatment. Other investigations include a plain abdominal radiography to check for calcified gallstones as a possible cause and a chest X-ray to check for signs of ARDS5- Definitive treatment- I would keep the patient NBM consider nutritional support (enteral or parenteral if severe) + good pain relief (PCA through a dedicated line)- I would request an USS to check for stones in the biliary
Causes of pancreatitis
GET SMASHED- Gallstones (most common cause in the UK)- Ethanol (second most common)- Trauma- Steroids - Mumps- Autoimmune disease- Scorpion bites- Hyperlipidemia , hyperacalcemia- ERCP- Drugs (thiazide diuretics)
What fluids to give in acute pancreatitis (surgical emergency)
The constituents ions of Hartmann’s solution are very similar to the ECF compartment. As pancreatitis leads to fluid loss, which is mainly ECF , replacing with an isotonic crystalloid seems the logical choice
How much fluid to give as resuscitation of acute pancreatitis
Patients should receive maintenance fluids plus additional losses. As this patient is likely to have suffered significant third space loss, it would not be unusual to give 6l or more in one dayHowever I would firstly need to assess the patient volume status and guide fluid replacement according to thatEmpirically I would give 1l stat followed by another 1l over the first hour, then another 1l over the subsequent 2 hours, another over the next 3 hours and then 6 hourly thereafter. This would be guided by the fluid balance chart which should be strictly kept
How would you assess the severity of the pancreatitis attack?
Using the Glasgow prognostic score (in the first 48 hours)- P: Arterial pO2 < 8 KAps- A: Age > 55- N: Neutrophiles > 15- C: Calcium < 2- R: Raised urea > 16- E: elevated enzymes AST> 125 or LDH > 600- A: Albumin < 32- A: Sugar > 10Score of 1: mildScore of 2: moderateScore of =>3: severe and is an indication for HDU Independent from the other variables, a CRP > 150 constitutes a severe attack
What are the different types of pancreatitis
- Oedematous (most common)- Haemorrhagic (look for Cullen’s sign or Grey Turner sign)- Necrotising pancreatitis
Would you start antibiotics in a acute pancreatitis
Use of antibiotics is controversial. Important to:- Follow trust protocol- In case of infected pancreatic necrosis, discuss with on call microbiologist and my seniors…
What diagnosis would you consider if a patient had a persistent raised amylase?
- pancreatic pseudocyst is the likely causeIt commonly occurs in pancreatitis due to alcohol and is conformed on CT scanThose< 6 cm in size resolve within 6 weeksLarger ones may need to be percutaneously drained under radiological guidance
How to manage a man with hematemesis?
- recognise its an emergency- Initial resuscitation: mainly assess level of hypovolemic shock- Emergency investigation: FBC, U&E (IF raised urea then recent GI bleeding), LFT, Amylase, clotting, cross match at least 4 units of blood- Additional monitoring: CVP line and catheter to accurately guide resuscitation- Call for help: “after Discussion with a senior colleague I would like to consider the need for an emergency OGD In the unstable patient.- Assess severity: rockall score (prognostic scoring system for acute GI bleeds based on the patient’s medical history, current clinical Condition and endoscopic findings)- Definitive treatment: 1- consider resuscitation with blood if still hypertensive 2- PPI (if known peptic ulcer disease) 3- emergency OGD for diagnosis and treatment 3- Sengstaken-Blakemore tube if massive bleeding and the patient is still awaiting definitive treatment 4- Surgery if uncontrolled bleeding, re-bleeding, recurrent hypotension or the bleeding site is not identified as OGD.NEVER FORGET TO CROSS MATCH BLOODAND PUT TWO LARGE BORE CANNULA IN ANTECUBITAL FOSSA
How to manage a man with hematemesis?
- recognise its an emergency- Initial resuscitation: mainly assess level of hypovolemic shock- Emergency investigation: FBC, U&E (IF raised urea then recent GI bleeding), LFT, Amylase, clotting, cross match at least 4 units of blood- Additional monitoring: CVP line and catheter to accurately guide resuscitation- Call for help: “after Discussion with a senior colleague I would like to consider the need for an emergency OGD In the unstable patient.- Assess severity: rockall score (prognostic scoring system for acute GI bleeds based on the patient’s medical history, current clinical Condition and endoscopic findings)- Definitive treatment: 1- consider resuscitation with blood if still hypertensive 2- PPI (if known peptic ulcer disease) 3- emergency OGD for diagnosis and treatment 3- Sengstaken-Blakemore tube if massive bleeding and the patient is still awaiting definitive treatment 4- Surgery if uncontrolled bleeding, re-bleeding, recurrent hypotension or the bleeding site is not identified as OGD.NEVER FORGET TO CROSS MATCH BLOODAND PUT TWO LARGE BORE CANNULA IN ANTECUBITAL FOSSA
What are the causes of an upper GI bleed
- duodenal ulcer (most common)- Gastritis, esophageal varices- Mallory-weiss tears - Malignancy
What ate the surgical options if bleeding is due to bleeding peptic ulcer
- under-running of the bleeding vessel- Excision of the ulcer- Gastrectomy
What are the causes of an upper GI bleed
- duodenal ulcer (most common)- Gastritis, esophageal varices- Mallory-weiss tears - Malignancy
What ate the surgical options if bleeding is due to bleeding peptic ulcer
- under-running of the bleeding vessel- Excision of the ulcer- Gastrectomy
What is the rockall score?
This is a prognostic scoring system for acute GI bleeding baSed on patients Medical history, current Clinical condition and endoscopic findings(Age, shock, co-morbidity, diagnosis, endoscopy)Score>8: high risk of deathSour<3: excellent prognosis
How to manage an acutely painful pulseless leg
Key features to mention:- Recognise that this is an emergency- Initial resuscitation: include iv fluids and opiate analgesia- Emergency investigations: angiogram in incomplete ischemia, DO NOT DELAY DEFINITIVE TREATMENT IF COMPLETE ISCHEMIA- additional monitoring: CVP line and catheter to accurately guide resuscitation- Call for help: call early as time is
What are the signs of acute limb ischemia
This is known as the 6 Ps- Pain: usually severe- Pallor: occurs in progressive stages (1- white appearance progressing to mottled but blanching 2- non blanching mottled skin 3- fixed staining and liquefaction- Perishingly cold- Pulseless (confirm with Doppler)- Paresthesiae (Assess sensation)- Paralysis (Assess motor function)PARESTHESIAE AND PARALYSIS ARE LATE SIGNS (USUALLY IRREVERSIBLE)
what specific post Op complications to look for
- Reperfusion injury: when arterial oxygen is reintroduced, leads to oxygen free radicals causing endothelial damage- Can lead to metabolic complications such as acidosis ARDS and myoglobinemia or it can lead to a compartment syndrome which requires emergency fasciotomy
This man was found collapsed in the street. He has a plausible expansile mass on abdominal examination. How would you manage him?
- recognise urgency- Initial resuscitation: includes blood (do not wait for cross match, give O-), maintain BP < 90, as it may destabilise a tamponading clot (permissive hypotension), two large bore cannula…- Emergency investigations: none required. Straight to theatre. 10 units needed…- Additional monitoring: CVP line and urinary catheter- Call for help- Definitive treatment: immediate Surgery to cross clamp the aorta proximal to the rupture and control the bleeding ITU care post operativelyA 60 YEAR OLD MAN WHO PRESENTS WITH RENAL COLIC CAN BE A LEAKING AAA.NEVER SEND AN UNSTABLE PATIENT TO CT SCAN. THEY MIGHT ATTEST
5 days Post hemicolectomy (for sigmoid ca). The nurses have called you as she has spiked temperature. How to manage Post operative fever?
- Recognise urgency- initial resuscitation: involves a quick systematic examination to look for a cause (listen to chest for basal atelectasis, examine the abdomen for peritonitis, look at wounds for signs of infections and examine the legs for DVT. Assess for SIRS (systematic inflammatory response syndrome)- Emergency investigations: do septic screen (FBC, urine dipstick, CXR, and blood culture before starting antibiotics. Consider water soluble contrast study of the rectum to rule out an anastomotic leak- Call for help- Definitive treatment: depends on cause/// NBM /// If urine or chest infection: give empirical antibiotics iv and chest physiotherapy for basal atelectasis. If patient in septic shock then give fluid challenge and consider HDU/// Anastomotic leak (occur between day 3 and d 5): if patient stable and leak is small them conservative management preferred. If peritonitic, then laparotomy for wash out and plug the leak
What is the most common cause of postoperative fever in abdominal surgery
Basal atelectasis. It can be prevented with good chest physiotherapy an nd airway adequate analgesia. That’s why some patients are kept on epidural analgesia to be able to take good deep breaths.
What are the causes of postoperative fever
- immediate < 24 hours: physiological stress response to Surgery- Early: /// < 3 days: basal atelectasis (pneumonia)/// > 3 days: pneumonia, wound infection, anastomotic leaks, subphrenic or pelvic abscess, UTI, line infection/// > 5 days: PE or DVT
What is SIRS?
systemic inflammatory response syndrome with at least 2 of the following features:- Temperature>38 or 90 minutes- Respiratory rate: > 20 / minute- White Cell count: > 12 or < 4
Woman returning to the Ward after having a laparotomy for acute abdominal pain. Hourly urine output<30 ml. How to manage postoperative oliguria?
- Recognise urgency- Initial resuscitation: quick systematic examination to assess volume status:/// Mental status (confusion)/// Hands (skin turgor, prolonged CRT, patient cool and clammy,?/// Vital signs: tachycardia, hypotension/// JVP: if low/// Examine: chest for signs of fluid overload, abdomen for distended bladder (in obstruction)/// Fluid balance chart assessment- Emergency investigations: renal function urea creatinine…- Additional monitoring: CVP monitoring if not responding to fluid challenges + urinary catheter…- Call for help- Definitive treatment: depends on cause/// Post renal: obstruction by large stove or BPH causing acute urinary retention/// intrinsic renal: call for expert (may need dialysis)/// Pre-renal: give fluid challenge and reassess. This is the most common cause of postoperative oliguria and is most likely due to hypovolemia secondary to dehydration.
Man involved in rta. No obvious sites of injury.
- Recognise urgency: manage according to ATLS principles- Initial resuscitation: intubation because gcs low (endotracheal tube)… Fluids… Anesthetits- Emergency investigations: CXR, pelvic x Ray c-spine. FAST scan to look for source of bleeding. CT head chest abdo pelvis if stable.- Additional monitoring: urinary catheter- Call for help- Definitive treatment: /// Identify source of bleeding by looking in 5 places: abdomen, chest, long bones/pelvis, head and floor/// If intra abdominal bleeding this will require immediate laparotomy to diagnose and treat
How do you assess hypovolemic shock?
Through Clinical examination and Assessment:- Stages of hypovolemia1- blood loss up to 15%2- 15-303- 30-404- > 40…Bp will only drop in phase 3
What is a FAST scan
Focused Assessment sonogram in traumaRapid because ultrasound examination of various parts of the body where blood is likely to have collected Post trauma. Looking at: abdomen, thorax…
Peripheral vascular examination
- General inspection: paraphernalia of disease: 1- does patient have an amputation? Describe level. Any associated walking/mobility aids or prosthesis? 2- is patient on oxygen, iv infusion of heparin, GTN spray and our cigarettes?- Upper limb vascular examination:1- examine hands: skin changes (tar staining, tendon Palmar xanthoma, purple discoloration of fingers (atheroembolism), muscle wasting (thoracic outlet syndrome), temperature, pulses, CRT, BP (less than 15 mmHg between 2 sides in absence of arterial disease)2- examine neck and face: eyes (corneal arcus, xanthelasma, conjunctivital pallor), mouth (central cyanosis & angular stomatitis), neck (prominent veins on neck, chest wall and over shoulders (indicates subclavian vein occlusion)), pulses (feel carotid pulse), bruits (auscultate for carotid bruits using bell of stethoscope).- Abdominal examination: Check for AS A- Lower limb vascular examination:1- General inspection: asymmetry (amputation, edema, muscle wasting), Surgical scars (indicative of previous varicose vein removal, or suggestive of vein harvesting for CABG, any varicosities present), skin changes (discoloration (erythema, pallor, Brown/hemosiderin deposits, purple/black from haemostasis), venous guttering, trophic changes(no hair, shiny skin, gangrene), ulcers2- closer inspection: detailed inspection of toes (amputation, purple discoloration (AAA trash foot), ulcers), focus on pressure areas where ischemic ulcers can develop (sole, lateral, heels…)3- palpation: Check skin temperature, CRT (if prolonged do a Buerger’s test, Buerger’s test (lift leg…). If PAD, then legs turn bluish from deoxygenated blood as it travels over ischemic tissues and then turns red from reactive hyperuremia from Post-hypoxic vasodilation. Check peripheral pulses (femoral (mid-inguinal point= halfway between ASIS and the pubic tubercle), popliteal pulse, posterior tibial pulse (posterior and 2 cm inferior to medial malleolus of tibia), dorsalis pedis pulse (lateral to extensor hallucis longus tendon, absent in 10%)4- auscultation: listen for bruits over femoral artery and over aorta and iliac barrels5- special tests: measure ABPI on both sides (>0.9 normal, 1.2 can suggest hardening of the arteries from calcification, resulting in arteries being stiffer or less compressible. Seen in patients with DM and renal failure.
How to investigate a peripheral artery disease patient?
Investigations can be divided into bedside tests, blood tests and imaging.1- simple bedside tests: BM (see if diabetic), ECG (for evidence of coexisting heart disease because patient likely arteriopath)2- simple blood tests: FBC (anemia, polycythemia), U&E (renal function, important if undergoing contrast studies, especially in diabetics (contrast-induced nephropathy), lipid profile, clotting, esr (vasculititdes), G&S (if operative management)3- imaging: ///”cxr to look for coexisting cardio Respiratory disease, particularly as part of a pre oPerative Assessment”. “I would like to request specialist imaging to assess the extent of disease and help plan operative management: duplex scan to check for the degree of stenosis. ///Spiral CT to reconstruct 3d images of vessels noninvasively. /// in some patients a digital subtraction angiogram (DSA) to demonstrate the level of blockage, runoff and presence of collateral blood supply.Management: those who undergo invasive imaging such as angiography have a catheter introduced (seldinger technique) into femoral artery and guided to site of lesion, where radio dense contrast is injected and imaged using x rays. Stenosis can be treated at same time by balloon angioplasty.
Can you estimate the extent of stenosis from a hand held Doppler probe
- Simple hand held Doppler probe detects arterial pulsation add an audible signal.- Degree of stenosis causes turbulent blood flow which results in bruits heard on auscultation with a stethoscope- Characteristic waveforms seen:/// Normal vessels: triphasic waveforms/// Mild stenosis: biphasic waveform/// Severe stenosis: monophasic waveform
Why are lower limbs more commonly affected by PAD compared to lower limbs
Arterial supply to legs is noir as well developed as the arterial supply to upper limbsTherefore th re lower limb arterial supply is also more susceptible to atherosclerosis than the upper limbs. So PAD is 8 times more common in lower limbs than in upper limbs
How to treat a patient with lower limb occlusive arterial disease?
This involves an MDT management approach. Conservative and Medical management focus around modification of risk factors and Surgical measures1- Conservative measures include: stopping
Benefits of a below-knee amputation (BKA) over an above knee amputation (AKA)
BKA are preferred:- Better mobility for patients and less likely to be ♿ bound- Physical benefits (reducing energy to mobilise)- Life expectancy better for BKA - Patients with AKA more likely to develop critical ischemia in other leg
Reasons for amputation?
Three Ds - Dead limb (vascular (PAD)- Dangerous limb (infection (osteomyelitis)- Debilitating limb (trauma (frostbite))
Please examine this man’s abdomen as part of your vascular examination
Key features to look for:-inspection: look for abdo scars, mainly over femorals (from previous bypass surgery), obvious mass in epigastrium, visible pulsations (kneel from side to see them)- Palpation/auscultation: /// Palpate above and slightly to left of the umbilicus (before aorta bifurcates at L4 level)/// See if pulsatile and expansile (one ✋ moves laterally with each pulse)/// Estimate transverse diameter of the mass in centimeters/// Try to feel the upper border of the mass, if felt it would suggest aneurysm is infrarenal (only 1% suprarenal)/// Auscultate aneurysm for bruits/// Examine femoral and popliteal pulses
Please examine this man’s abdomen as part of your vascular examination
Key features to look for:-inspection: look for abdo scars, mainly over femorals (from previous bypass surgery), obvious mass in epigastrium, visible pulsations (kneel from side to see them)- Palpation/auscultation: /// Palpate above and slightly to left of the umbilicus (before aorta bifurcates at L4 level)/// See if pulsatile and expansile (one ✋ moves laterally with each pulse)/// Estimate transverse diameter of the mass in centimeters/// Try to feel the upper border of the mass, if felt it would suggest aneurysm is infrarenal (only 1% suprarenal)/// Auscultate aneurysm for bruits/// Examine femoral and popliteal pulses
Please examine this man’s abdomen as part of your vascular examination
Key features to look for:-inspection: look for abdo scars, mainly over femorals (from previous bypass surgery), obvious mass in epigastrium, visible pulsations (kneel from side to see them)- Palpation/auscultation: /// Palpate above and slightly to left of the umbilicus (before aorta bifurcates at L4 level)/// See if pulsatile and expansile (one ✋ moves laterally with each pulse)/// Estimate transverse diameter of the mass in centimeters/// Try to feel the upper border of the mass, if felt it would suggest aneurysm is infrarenal (only 1% suprarenal)/// Auscultate aneurysm for bruits/// Examine femoral and popliteal pulses
potential complications of AAA
- rupture, dissection, thrombosis and embolisation from the thrombosis leading to trash foot- Fistula formation into adjacent organs, such as the colon (mainly duodenum) our vena cava
What is a fistula?
It’s an abnormal connection between two epithelial surfaces lined by granulation tissue
What factors to make you consider elective operative treatment of an aneurysm
Depends on two features: symptomatic or not/// Asymptomatic: recommendation for repair when aneurysm diameter is >5.5 cm or if expanding at rate of > 1 cm a year/// Symptomatic patients should have their aneurysm repairedTypes of AAA repair:- Endovascular repair (can be done by interventional radiologist- Open repair
What do you know about the NHS AAA screening programme
If you are a man aged over 65 you are more likely to have an abdominal aortic aneurysm. That is why the NHS AAA Screening Programme invites men for screening during the year (1 April to 31 March) that they turn 65.Men over 65 who have not previously been screened or diagnosed with an aneurysm can request a scan by contacting their local programme directly.Good screening programme needs to meet the Modified Wilson’s criteria for screening programmes (the condition should be an important health problemthe natural history of the condition should be understoodthere should be a recognisable latent or early symptomatic stagethere should be a test that is easy to perform and interpret, acceptable, accurate, reliable, sensitive and specificthere should be an accepted treatment recognised for the diseasetreatment should be more effective if started earlythere should be a policy on who should be treateddiagnosis and treatment should be cost-effectivecase-finding should be a continuous process)
Draw the arterial vessels of the body
….
Draw the venous system of the body
Lower limbs: 1- superficial system: long and short saphenous veins. Responsible for draining the skin and subcutaneous tissues of the leg2- deep venous system: exists within the muscles of the leg and is covered by fascia. Receives blood from superficial venous system through the connecting perforation veins. When muscle contracts, blood pushed towards the ❤ and valves in veins are responsible for preventing backflow of blood. If valves incompetent, blood is forced from deep system to superficial system, causing veins to dilate.
Definition of varicose veins
Dilated tortuous and prominent veins of the superficial venous system of the lower limb seen in the distribution of the short and long saphenous veins
Risk factors for Development of varicose veins
History of dvt/pe Increasing ageObesityPositive family historyPregnancy and pelvic masses (cause increase pressure on the ivc and iliac veins)Any previous treatment to the legOCP use (needs to be stopped at least 4 weeks before any Surgical intervention due to risks of DVTAsk in history about aching legs and swellings, legs feeling heavy, pruritus, restless legs and skin changes (venous eczema, ulcers). Symptoms usually worse at night, and in occupation that requires standing o
Clinical examination of varicose veins
ALWAYS REMEMBER TO EXAMINE PATIENT ERECT AAD VARICOSITIES MIGHT BE COLLAPSED IF SUPINE 1- introduction: patient spine initially then patient required to stand up2- inspection:/// Observe patIent lying spine: - General inspection (any obvious asymmetry, scars from previous varicose veins removal or vein harvesting for CABG, any varicosities), - signs for chronic venous insufficiency (1- swelling and brown discoloration/hemosiderin deposition, 2- telangiectasia and venous eczema, 3- lipodermatosclerosis from chronic venous hypertension causing sclerosis of skin and subcutaneous tissues from fibrin deposition 4- erythema seen in thrombophlebitis.- Look in gaiter area around medial malleolus (where venous ulcers are typically seen)- Look at groin for hernias, saphena varus or prominent lymph node/// Observe patient standing: look for tortuous varicosities (anteriorly for long saphenous and posteriorly for short saphenous). “Posteriorly I can see that there are multiple dilated and elongated veins in the distribution of the short saphenous vein”. PATIENT REMAINS STANDING UNTIL TOURNIQUET TEST3- Palpation /// Palpate for a saphena varix (locate SFJ which is 2 cm inferior and 2 cm medial to femoral pulse (at mid-inguinal point). If lump found, might be a saphena varix which will be smooth with a palpable thrill and will empty on minimal pressure and refill once fingers are removed/// Cough test: place 2 fingers on SFJ while patient standing, if thrill felt then incompetence of valve. DO COUGH TEST AFTER CHECKING FOR SAPHENA VARIX./// Palpate varicosities: press and release and see refill. If pain then phlebitis. If vein feels hard, then thrombosis./// Palpate to check temperature4- special tests: to determine site of incompetence/// Tap test: find prominent varicosity. One hand over SFJ and other over varicosity. Tap over SFJ. If thrill transmitted to varicosity… Suggests incompetence at SFJ./// Trendelenberg / tourniquet test: in supine position, raise leg to comfortable angle for patient and you. Milk leg. Then tourniquet as high as possible. Patient stands. If veins refill immediately: level of incompetence below SFJ (repeat with tourniquet lower, mid-thigh, calf)). If veins do not fill: level of incompetence above tourniquet i.e. at SFJ./// Doppler probe: most reliable of the special tests. Place Doppler over SFJ. With other hand squeeze calf. And listen to the”whoosh” sound coming from probe. In normal leg: only hear noise once as blood forced proximal. In SFJ incompetence, double whoosh (second heard because blood flows backwards through valve when stop squeezing the calf). Repeat at saphenopopliteal junction.5- Auscultate: listen for bruits over varicositiesTo compete my examination, I would like to Palpate for peripheral pulses and examine the abdomen as well as perform a DRE to exclude an abdominal or rectal mass.IT’S IMPORTANT TO CONSIDER SECONDARY CAUSES OF VARICOSE VEINS, PARTICULARLY MALIGNANCIES.
Where to locate the SFJ (saphenofemoral junction)
4 cm below and 4 cm lateral to public tubercle
describe the course of great and short saphenous vein?
- great saphenous vein: passes anterior to medial malleolus, travels proximal in medial aspect of the calf to the popliteal fossa and then travels along medial aspect of thigh to join the common femoral vein at SFJ - Short saphenous vein: arises posterior to lateral malleolus and ascends along the midline of the calf to join the popliteal vein in SFJ in popliteal fossaDON’T SAY VEINS START AT SFJ. STAY DISTALLY
how to investigate a varicose veins patient
- rule or secondary causes, ie abdominal/pelvic malignancies, DVT- Color duplex scanning with mating of perforators
How do you manage a varicose veins patient
Management involves- Taking a focused history to rule or secondary causes of varicose veins- Thorough clinical examination- Tailoring of investigations depending on findings before mentioning treatment options.Treatment can be conservative, medical or surgical- Conservative: treaty underlying cause if any (e.g. weight loss in obese, constipation…), Graduated compression stockings for symptomatic relief (TED stocking: thromboembolic disease)- Surgical measures/// Injection chemotherapy for small varicosities/// Multiple stab avulsions with vein stripping and ligation of the incompetent junction/// Subfacial endoscopic perforator Surgery (SEPS)/// radiofrequency or foam ablation
Possible differential diagnosis for varicose veins
- cellulitis, DVT - Phlebitis: inflammation of superficial veins, secondary to intraluminal thrombosis. If migratory, then raise suspicions about underlying malignancy- Osler-weber-rendu syndrome (telangiectasia, recurrent epsitaxis)
Tell me about DVT prophylaxis for surgical patients
I will take a history to assess for the presence of risk factors such as age, ocp use, smoking, previous history of DVT/PE and high risk surgical procedures associated with DVT (eg TKR (incidence=50%)).Main DVT prophylaxis:- TED stockings- Low Molecular weight heparin
Why is it important to check for history of DVT in patients undergoing varicose vein surgery?
- varicose veins may be secondary to thrombosis of the deep or superficial veins- If deep venous system not functioning, particularly after a DVT, patient is relying on the superficial system for venous return- Patients should have Doppler ultrasound scanning of their deep veins to confirm patency and check valve competence prior to Surgery- Clinically could perform a perthes test (put elastic bandage from toes to upper third of thigh to obliterate superficial veins. Ask patient to walk for 5 min. If deep system ok, nothing will happen. If incompetent, then pain in leg.
If the patient with varicose veins has an unusual rash on his face, what diagnosis to consider
Varicose veins associated with a port wine stain and limb hypertrophy are signs seem in the rare Klippel-Trenaunay syndrome.
Different types/causes of ulcers
Most common:- Arterial disease- Venous insufficiencyOther:- peripheral neuropathy- Trauma- Neoplastic causes: eg marjolin’s ulcer (an scc in long standing Non healing ulcer) eg in previous trauma or wound- Systemic disease (uc, ra), leading to pyoderma gangrenosum
Clinical examination of an ulcer
1- introduction: it’s acceptable to ask the patient at this point whether the ulcer is painful (helps in diagnosis)2- inspection/// General inspection of lower limbs: ? Signs of chronic venous insufficiency, varicose veins, trophic changes, amputations or surgical scars/// Describe site of ulcers- Arterial: pressure areas, tips of toes- Venous: gaiter area- Neuropathic: heel, on the sole under the metatarsal heads/// Describe size and shape of ulcer: estimate size in cm. Check shape to see if margins well defined or irregular- Arterial: small (few cm)- shape: well defined margins with regular outline- Venous: variable in size (can be very large). Shape: irregular outline and variable shape- Neuropathic: size: variable (several cm). Shape: regular outline/// Describe edge of ulcer- Arterial: punched out- Venous: sloping or flat- Neuropathic: punched out /// Describe base of ulcer: resonate depth of ulcer (sometimes can see underlying bone and tendons). Base can be from healthy to completely avascular.- healthy: pink granulation tissue, areas of epithelialisation- Sloughy: offensive, exudative discharge, usually green or yellow in color- Necrotic: black dead tissue- Avascular : shiny paleIF YOU SEE DISCHARGE, SAY TO EXAMINER THAT YOU WOULD TAKE SWABS FOR MC&S (MICROSCOPY CULTURE AND SENSITIVITY)AND START TOPICAL ANTIBIOTICS3- Palpation/// Check if painful (Neuropathic: no pain/ arterial and venous painful, but usually arterial more painful and require opiate analgesia)/// Check temperature of surrounding skin: Arterial: if colder than rest of leg. Venous: if warmer than rest of leg/// Check CRT: Arterial: prolonged crt /// Check peripheral pulses (mainly distal pulses)To complete my examination I would like to perform a complete peripheral vascular examination, looking particularly at sensation.
Definition of gaiter area
It’s the distal one third of the leg along the medial aspect, above the medial malleolus
What is granulation tissue (in the vascular context)
Granulation tissue is a heterogeneous structure that forms within the extracellular matrix at the end of the proliferative phase of wound healing. It consists of fibroblasts, macrophages and endothelial cells with a rich capillary network
What is a sloughy tissue (in vascular context)
This is most necrotic tissue
Please examine the lesion on this patient’s leg (Venous ulcer on gaiter area)
Key features to look for:- Inspection:/// Associated paraphernalia: treatment on table (topical antibiotic), for of bed raised (part of ulcer treatment), patient’s last bandage next to bedside/// General inspection of leg: patient usually an arteriopath, look for signs of chronic venous insufficiency or varicose veins. “On general inspection, the lower limbs are Oedematous with loss of hair, areas of hemosiderin deposition and lipodermatosclerosis. Site: gaiter area, size/shape: variable in size, can be extremely large, irregular margins. Edge: sloping. Base: shallow and sloughy with underlying pink granulation tissue./// Palpation: temperature: skin surrounding ulcer is warmer than the rest of the leg. Usually painless./// Completion: offer to examine for varicose veins as an associated feature. Offer ABPI. An index of >0.8 is prerequisite top compression bandaging. “I would like to check the patient’s ABPI to ensure the index is greater than 0.8 as the patient is likely to require four layer compression bandaging as part of his treatment”.i
What is lipodermatosclerosis and hemosiderin ?
It’s a skin and connective tissue disease. Known as chronic panniculitis with lipomembranous changes. An inflammation of the layer of fat under the epidermis.Hemosiderin deposition: common late complication of untreated superficial venous insufficiency or venous reflux resulting in chronic venous hypertension. Buildup of venous pressure in the superficial dilated veins leads too leakage of red blood cells from the capillaries into the surrounding tissues under the skin. Over time, breakdown of haemoglobin content of the red blood cells in these tissues lead to accumulation of hemosiderin, resulting in long term and potentially permanent brown pigmentation of the overlying skin. (Potential treatment: intense pulse light (IPL) and tattoo removal lasers)
What is compression bandaging
This is part of the treatment for venous ulcers and most ulcers heal within a year with this treatmentEvidence based medicine proves that compression bandaging works, it should be offered to all patients with an ABPI>0.8 (because they could otherwise compromise arterial flow to the limb. It’s a four layer bandaging technique (Non adherent dressing over the ulcer, followed by crepe bandage, blue lien bandage and finally an adhesive bandage).
What to consider if venous ulcer fails to heal
“The great majority of ulcers heal by 12 weeks and most heal by a year. So if an ulcer fails to heal, I would need to consider the possibility of malignant transformation of a long-standing ulcer and arrange for a biopsy to exclude a marjolin’s ulcer.Always say MDT management (including wound Care Nurse, OT, district Nurse Care…)In conservative management: patient advised to rest and keep limb elevated to reduce venous hypertension. Once ulcers are healed, patient advised to wear graduated elastic compression stockings.Surgical: skin graft may be used with excitation of the underlying dead skin.
Please examine the lesion on this patient’s foot (Arterial ulcer)
Key features to look forInspection://// Associated paraphernalia: patient may be on prostaglandin infusion/// General inspection of the leg: patient usually arteriopath. If amputation on opposite limb them mention it./// Site: usually on pressure areas of feet, around the toes)/// Size/shape: well defined regular margins, size no more than several cm/// Edge: classically punched out/// Base: no granulation tissue due to poor blood supply. May be necrotic or Avascular. Can be deep. Even potentially see tendons and bone. “The ulcer appears deep and I cam see the underlying bone”- Palpation: temperature (surrounding skin cold and grayish blue discoloration), painful ulcer (may be masked by peripheral neuropathy in diabetics. Peripheral pulses absent (offer to use a Doppler probe, loss of triphasic waveform seen in arteriopath).Completion/management:Management similar to those for peripheral vascular disease. PAIN RELIEF IS KEY (WHO pain ladder). Use of vasodilators such as prostaglandins or surgical techniques such as lumbar sympathectomy.
How to distinguish ivc obstruction from portal hypertension
, look at veins below umbilicus
When to consider pleuridesis
2 or more spontaneous pneumothorax
Tell me about bone scan
Radioisotopes caught by more metabolically active…
Definition of laparotomy
Inspection of…. Check
Difference between arterial claudication and neurological claudication (spinal stenosis)
Other types of claudicationNeurological: spinal stenosis (numbness, worse on bending forward),
What do claudication patients die of
Mi cva renal failureMortality 5y 60%Give antiplatelets and statin
Definition of critical ischemia
3 parts Greater than 2 weeks Rest pain unremittingTissue lossAbpi less than 0,5
Acute ischemia
PalePulselessPerishing coldPainfulParasthesiaParalysis
How do aneurysms present
Incidental findingNerve compression/painVein compression/dvt (popliteal aneurysm)Embolisation or thrombosisFistula (aorta enteric fistula, aorta cutaneous fistula, aorto cava fistula)
Screening for aaa
> 65One of uss of abdomen
Complications of aneurysms
RuptureEmbolisation (trash footThrombosis (acutely ischemi, leg)Pressure DVTFistularion acutely unstable usually
Thoracic outlet syndrome
Venous: upper limb dvt and long term swellingArterial: raynaud, claudication embolisationNeurological: pain radiculipathyIx: mri, mra MarcDuplex in abductionNerve conduction studies
Why do diabetics get ulcer
Pvd Small vessel diseaseNeuropathyInfection
What is a charcot joint
Painless… Check definition
Causes of raynaud
CrestThoracic outlet syndromeIdiopathic (Primary) most common white blue redLarge vessel diseaseVasculiticOccupational: vibrating toolIatrogenic: anthocyaninsHaematological: polycythemia, cold affliction.
How to estimate area of body surface burntWhy is it important to know
Rule of 9If more than 15% them start fluid resuscitationManagement with split-skin graft taken from thigh
Common nerve lesions in carotid artery Surgery
Hypoglossal nerve palsy (tongue towards lesion)Recurrent laryngeal 9 (cough)…8710
Describing fracture radiograph
See photo
Management of fractures
ResussReduce restrict/hold Rehabilitate
Smith and colles fracture
Smith’s fracture, also sometimes known as a reverse Colles’ fracture or Goyrand-Smith’s, is a fracture of the distal radius.[1] It is caused by a direct blow to the dorsal forearm[2] or falling onto flexed wrists, as opposed to a Colles’ fracture which occurs as a result of falling onto wrists in extension. Smith’s fractures are less common than Colles’ fractures.The distal fracture fragment is displaced volarly (ventrally), as opposed to a Colles’ fracture which the fragment is displaced dorsally. Depending on the severity of the impact, there may be one or many fragments and it may or may not involve the articular surface of the wrist joint.
Most likely cause of postoperative pyrexia, tachycardia and dyspnea
Postoperative pulmonary collapse. Extremely common following thoracic abdominal or groin Surgery.Pyrexia unlikely from wound infection our PE so soon after surgery.Cause: retention of plugs of mucus in bronchial tree.Managed Physio, vigorous breathing exercises, coughing in upright position, passion management pca, antibiotic
Burst abdomen = abdominal wall dehiscenceFactors- causes
FolloWing colectomy…Usually preceded by pink fluid sign, serous peritoneal exudate from wound several days before complete dehiscence.Factors:Preoperative factors: vit c deficiency, protein deficiency, jaundice, uremia, anemia, chronic cough, abdominal distensionOperative factors: faulty techniquePostoperative factors: cough abdominal dissension, wound sepsis
Managing burst abdomen
Reassure patient or relativesIv morphine as sedation and pre anesthetic medication and antiemeticCover exposed viscera and transfer to theatre with General anesthesia
What happens with incisionsal hernia
Deep layers of abdominal wound give eau but skin sutures hold
Definition of fistula
Pathological communication between two epithelial surfaces
Fistulogram
Injection of radioopaque contrast fluid gastrograffin through fine catheter into the fistula
Definition of cellulitis
Spreading infection of cellular tissues. May involve superficial fascia, overlying skin…Symptoms: heat pain redness swellingComplications: abscess + homogeneous ,+ systemic features like Pyrexia ill Management: swab blOod culture antibiotics
Definition of abscess
It’s a localised collection of pus. Pus is defined as living and dead phagocytes usually containing living and dead bacteria.
General manifestations of an abscess
Swinging PyrexiaTachycardiaMalaiseAnorexiaSweating Polynorph leucocytosisSometimes pus seen around a piece of suture: stitch abscess
Carbuncle
Area of subcutaneous necrosis that discharges onto the surface through multiple sinuses. Most commonly neck from collar excoriatingUsually staph aureus Common in diabetics
Indications of renal transplant
Check
Sister Marie Joseph nodule
Intra abdominal and ovarian cancer
Recti
Lines alba
Hydrocele
Fluid in tunica vaginalis
Hematuria causes
Check
Bladder cancer
Majority transitional Cell cancerScc: shistosomiasis
JJ stent
A ureteral stent, sometimes as well called ureteric stent, is a thin tube inserted into the ureter to prevent or treat obstruction of the urine flow from the kidney. The length of the stents used in adult patients varies between 24 to 30 cm. Additionally, stents come in differing diameters or gauges, to fit different size ureters. The stent is usually inserted with the aid of a cystoscope. One or both ends of the stent may be coiled to prevent it from moving out of place, this is called a JJ stent, double J stent or pig-tail stent.
Definition of urinary retention
Painful palpable our percussavle bladder when the patient us unable to pass any urine Inability of passing urine
Contents of spermatic cord
Arteries: testicular artery, deferential artery, cremasteric arteryNerves: nerve to cremaster (genital branch of the genitofemoral nerve), testicular nerves (sympathetic nerves) and the ilio-inguinal nerve- Ilio-inguinal nerve not inside spermatic cord, but runs along the outside.Vas deferens (ductus deferens)Pampiniform plexusLymphatic vesselsTunica vaginalis (remains of the processus vaginalis)
Borders of inguinal canal
Superior wall (roof): 2 Muscles:internal oblique Muscletransverse abdominus MuscleAnterior wall: 2 Aponeuroses:Aponeurosis of external obliqueAponeurosis of internal obliqueLower wall (floor): 2 Ligaments:inguinal Ligament·lacunar LigamentPosterior wall: 2Ts:Transversalis fasciaconjoint Tendon
Hesselbach triangle
RIPMedial border: Lateral margin of the rectus sheath, also called linea semilunarisSuperolateral border: Inferior epigastric vesselsInferior border: Inguinal ligament, sometimes referred to as Poupart’s ligament
Midline laparotomy
Skin, fat, linea alba and peritoneum
Femoral triangle
The femoral triangle is bounded:superiorly by the inguinal ligament.medially by the medial border of the adductor longus muscle.laterally by the medial border of the sartorius muscle.[2]
Focused Hx in skin presentation
- duration: how long it’s been present- changing lesion: changed, increased, decreased, disappeared then reappeared? Seasonal? Bleeding? Itching?- inheritance: FH?- environmental influence: occupation and hobbies. Sun? Sun Beds?- Drug side effect: patient taking any meds?- hypersensitivity: any known allergies- pt HX: anything like this before? How was it treated?
What are the muscles of the eyelids
Orbicularis oculi (facial nerve 7): closes eyeLevator palpebrae: (CN3): opens eye
CN in medulla
9 10 11 12
CN in pons
5 6 7 8
Swinging light test
RAPD relative afferent pupillary defectAka Marcus Gunn pupil
Eye muscles
Superior rectus: 45 lateralInferior rectus: 135 lateral Medical rectus: 90 medialLateral rectus: 90 lateralSuperior oblique: 135 medial Inferior oblique: 45 medial
Cranial nerve 4 palsy
Muscle involved: trochlear / superior obliqueEffect: head tilt away, hypertropia (up tilt and away from lesion… Very subtle. Eye moves up when horizontal H examination). Double vision when reading book or walking down stairsCauses: vasculitic (diabetes hypertension), trauma, congenital, tumour
Cranial nerve 3 palsy
Lateral rectus muscle and levator muscleEffect: down and out+ pupil dilationCauses: vasculitic ( diabetes, hypertension) aneurysms
Cranial nerve 6 palsy
Abducens muscleEffect: crossed eyes (double vision when looking towards affected eye)Causes: vasculitic (diabetes, hypertension), increased intracranial pressure
Patient with horizontal diplopia and lots of hearing. Where is the lesion
If CN3, then down and out which is not the case hereSo probably CN6 (loss of hearing 7) so probably in pons
No eye movement at all+ good vision+ loss of sensation in cheek and brow. Where is the lesion?
Cavernous sinus lesion causing problems with CN 3 4 and 6 and V1 and V2 of CN5
Definition of angina and how to differentiate it from MI
Angina is a term used to describe cardiac chest pain resulting from myocardial infarctionAngina usually lasts less than 20 min, is relieved by rest and by GTNvsMI tends to be longer, lasting more than 20 min and can last several hoursELDERLY AND DIABETICS CAN HAVE SILENT MI
Apart from chest pain, how can cardiac patients present
Symptoms of cardiac failure such as:
- SOB
- Orthopnea
- Paroxysmal Nocturnal Dyspnoea (PND)
- Ankle swelling
What is PND
Paroxysmal nocturnal dyspnea(orPND) refers to attacks of severeshortness of breathand coughing that generally occur at night.It usually awakens the person from sleep, and may be quite frightening.Though simpleorthopneamay be relieved by sitting upright at the side of the bed with legs dependent (legs dangling),in a patient with paroxysmal nocturnal dyspnea, coughing and wheezing often persist even in this position.
How might cardiac conduction abnormalities manifest in symptoms?
- Palpitations
- Chest pain
- Syncope
Possible causes of palpitations?
- AF
- VT
- SVT
Define syncope
Syncope is a transient loss of consciousness usually due to inadequate cerebral perfusion
What are the cardiac causes of syncope?And the other important but sometimes overlooked causes of cardiac syncope?
Cardiac causes include:
- AF
- Paroxysmal tachycardias
- Ventricular tachycardias
- Heart block (I, II, III)
- slow arrhythmia (sinus brady)Other: HAPE mnemonic
- HOCM (hypertrophic obstructive cardiomyopathy)
- Aortic stenosis
- PE (important prognostic factor in PE)
- Atrial myxomaSlow arrhythmia
What to ask for in the FH section in the CV history taking?
Non-modifiable risk factor:
- Early death
- FH of peripheral vascular disease
- FH ofischemic heart disease
- FH of stroke
- FH of hypertension
- FH of hyperlipidemia
- FH of sudden death !!!!!!!!
What to ask about in the Drug history section in CV history taking?
- OTC drugs
- Recreational drugs such as cocaine (cause chest pain)
- Check if asthmatic cause relative CI to beta blockers
- Check if there is Hx of peptic ulcer disease… It’s an important negative. might be prescribing aspirin.
What are splinter hemorrhages?
these are vasculitic lesions under the nail. Seen in endocarditis.
What are osler’s nodes and Janeway lesions?
- Osler’s node: finger pulp - Tender
* Janeway lesions: Palms - PainlessBoth seen in Endocarditis
Causes of raised JVP?
- CCF
- Cor pulmonale
- Tricuspid regurgitation
- Pulmonary hypertension
- Complete heart block
Describe the different waves in the JVP
- a wave: atrial contraction. Dissapears in AF
- c:tricuspid contraction
- x: atrium relaxes
- v wave: atrial venous filling (in tricuspid regurgitation)
- y: atrial emptying
What are the different eponymous signs of Aortic regurgitation?
- Watson’s water hammer pulse (collapsingpulse)
- Corrigan’s pulse(rapid upstroke and collapse of thecarotid arterypulse)
- lowdiastolicand increased pulse pressure
- de Musset’s sign(head nodding in time with the heart beat)
- Quincke’s sign (pulsation of the capillary bed in the nail; named forHeinrich Quincke)
- Traube’s sign(a ‘pistol shot’ systolic sound heard over the femoral artery; named forLudwig Traube)
- Duroziez’s sign(systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethoscope)
What signs can be elicited in the eyes in a CV examination?
- Corneal arcus Argyll Robertson pupil (syphillis) (not reactive/no constriction to light = prostitute pupil) (small, irregular pupils,the size of the pupils may be unequal,absence of the light reflex,a prompt accomodation reflex)
- Xanthelasma
- Conjunctival pallor
What are Thrills and Heaves
- Thrills: palpable murmurs
* Heaves: palpable beats (usually right ventricle hypertrophy)
What else to mention in a CV examination as other things to do/examine?
- lungs (for crackles), sacrum and ankle oedema Abdomen:
- for tender pulsatile liver (cardiac failure or tricuspid regurgitation)
- spleen for splenomegaly (infective endocarditis)
- Tender pulsatile mass indicative of AAA
- Auscultate for renal artery stenosis bruit
- Palpate for peripheral pulses
- Look for radiofemoral delay and auscultate over femoral arteries (aortic regurg)
- Examine the fundi for diabetic and hypertensive retinopathy, + look for Roth spots (IE) Dipstick urine for:
- Proteinuria (hypertensive retinopathy)
- Glycosuria (DM)
- Haematuria (IE)
Causes of heart murmurs
DR PECCS (mnemonic):
- Degenrative
- Rheumatic fever
- Prosthetic
- Endocarditis
- Congenital
- Connective tissue disease
- Syphillis (aortic regurg)
What are the non-modifiable risk factors for coronary artery disease?
- age
- sex
- family history
Name some modifiable risk factors for coronary artery disease
- smoking
- DM
- Dyslipidemia
- HTN
- Obesity
- Sedentary lifestyle
Symptoms of MI
- Chest pain at rest (rather on exertion) (often radiating to jaw, neck or L arm)
- Nausea
- Vomiting
- Sweating
- Collapse or SOB (if reduction of CO)DM sometimes no pain and N&V are the prominent symptom
Differentiate between the different acute coronary syndromes
- ACS: ischemic chest pain at rest or on rapidly reducing levels of exertion
- Unstable angina is pain without an enzyme rise (without evidence of necrosis)
- NSTEMI: chest pain with positive markers of necrosis (ie troponin) but without ST elevation
- STEMI: chest pain with ST elevation on ECG
Reliable examination findings in ACS?
Possible “autonomic features”:
- clamminess
- sweating
- Evidence of cardiogenic shock (shut down peripherally, hypotensive)
- Heart failure: crepitations, raised JVPSometimes not much is found on examination
What do ECG changes indicate in ACS?
ST elevation on ECG indicate full-thickness ischemia (STEMI).
- Usually due to thrombosis of an unstable plaque in a coronary artery leading to total occlusion
- Subtotal or transient occlusion generates partial thickness ischemia and this is represented on an ECG with ST depression or T wave abnormalities.Management:
- STEMI: Emergency reperfusion therapy (PAMI: Primary angioplasty in acute MI)
- NSTEMI: require angiography as well but pt can be stabilised medically.
Complications of ACS
Depending on the damage to the heart, there may be:
- evidence of shock = poor prognosis structural complications:
- infarction of mitral valve papillary muscles leading to acute mitral regurgitation
- rupture of the intraventricular septum causing VSD
- rhythm disturbances common. heart failure (serious and long term complication)
- function of ventricle impaired by presence of non contracting scar
What Rx to give on presentation of ACS?
- Aspirin (usually long-term)
- Clopidogrel (usually for 1 year)
- Enoxaparin (clexane)
- statin
- ACEI
- beta-blocker (if no CI)
Characteristics of unstable angina
- Chest pain at rest
- chest pain getting worse with exertion (reduced exercise tolerance)
- new onset chest pain
When is troponin measured?
12 hours from peak of pain (in practice on admission and 12h after).Troponin is used in risk stratification
What are the different cardiac biomarkers?
- Myoglobin (quickly)
- CK-MB
- LDH
- BNP
Complications of MI?
Mnemonic FAM
- Failure
- Arrhythmias (commonest VT & VF… require cardioversion
- Murmur: MR or VSD
Approach to systolic murmurs
- Chest pain… Likely AS
- Chest pain + Palipitations… Likely Mitral
- Chest pain + Dizziness… Likely AS
What are the main causes of Aortic stenosis?
- Calcific / degenerative AS : common with aging population (associated with atherosclerotic RF). Elderly >70
- Rheumatic heart disease (fusion of the commissures)
Most common symptoms of AS?
- Angina (often first symptom)
- Syncope
- Heart failure (breathlessness, oedema)
Signs of AS?
- Ejection systolic murmur in aortic region (R sternal edge) heard in carotids
- Apex hyperdynamic
- Slow rising pulse
- Low volume
Typical ECG findings of AS?
Resistance to outflow through the left ventricular outflow tract caused LVH.
Treatment options for AS?
- Medical: no evidence Surgical:
- Symptomatic AS: Valve replacement (gold standard)
- Asyptomatic AS: regular annual fup with serial echo
- IN OLDER PATIENTS, DO ANGIOGRAPHY BEFORE VALVE REPLACEMENT
What drug class not to use in patients with severe AS?
Never give NITRATES in severe AS as they reduce preload which will impact the cardiac output
What is valvuloplasty?
It involves inserting a balloon across the valve and inflating it to increase the size of the stenosed valve orifice.Doesn;t increase survival and risk of complications
What is a TAVI?
- Transcatheter aortic valve implantation
- Under GA, catheter inserted accross stenosed aortic valve (through apex of the heart or from femoral arteries).
- In catheter, there is expandable valve opens in the old stenosed valve, crushing the calcified old leaflets.
- Used for patients with unacceptably high risks of open valve replacement.
Prognosis of AS if untreated?
- Asymptomatic patients: very good Px Symptomatic patients: median survival of 2 years if untreated
- clinical features of HF are a late sign and carry worse prognosis.
What is the difference between aortic stenosis and sclerosis (classical final Q)
Sclerosis:
- No radiation
- Normal pulse
- Normally elderly
What advice to give when discharging a patient with AS?
Advice on:
- Symptoms: chest pain, syncope, cardiac failure
- Complications: HF
What is cardiogenic shock?
The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Cardiogenic shock is the leading cause of death in acute MI, with mortality rates of up to 70-90% in the absence of aggressive, highly experienced technical care.Signs and symptoms:The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing the following:
- Hypotension
- Absence of hypovolemia
- Clinical signs of poor tissue perfusion (ie, oliguria, cyanosis, cool extremities, altered mentation)
Features of Pancoast syndrome?
Pancoast syndrome is characterized by a malignant neoplasm of the superior sulcus of the lung (lung cancer) with destructive lesions of the thoracic inlet and involvement of the brachial plexus and cervical sympathetic nerves (stellate ganglion).This is accompanied by the following:
- Severe pain in the shoulder region radiating toward the axilla and scapula along the ulnar aspect of the muscles of the hand
- Atrophy of hand and arm muscles
- Horner syndrome(ptosis, miosis, hemianhidrosis,enophthalmos)
- Compression of the blood vessels with edema
Signs of portal hypertension
- Ascites
- Hepatic encephalopathy.
- Increased risk ofspontaneous bacterial peritonitis.
- Increased risk ofhepatorenal syndrome.
- Splenomegaly(enlargement of the spleen) with a consequent accumulation ofred blood cells,white blood cells, andplatelets together leading to mildpancytopenia.
- Portacaval anastomoses:Esophageal varices,gastric varices,anorectal varices andcaput medusae. Esophageal and gastric varices pose an ongoing risk of life-threatening hemorrhage, withhematemesisormelena.
Causes of ascites
Causes of highSAAG(“transudate”) are
- Cirrhosis- 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
- Heart failure- 3%
- Hepatic venous occlusion:Budd-Chiari syndromeorveno-occlusive disease
- Constrictive pericarditis
- Kwashiorkor(childhood protein-energy malnutrition) Causes of low SAAG (“exudate”) are:
- Cancer(primary peritoneal carcinomatosis and metastasis) - 10%
- Infection:Tuberculosis- 2% orSpontaneous bacterial peritonitis
- Pancreatitis- 1%
- Serositis
- Nephrotic syndrome
- Hereditaryangioedema Other Rare causes:
- Meigs syndrome
- Vasculitis
- Hypothyroidism
- Renal dialysis
- Peritoneum mesothelioma
Stages of diabetic retinopathy
Diabetic retinopathy has fourstages:
- Mild Nonproliferative Retinopathy.At this earliest stage, microaneurysms occur. They are small areas of balloon-like swelling in the retina’s tiny bloodvessels.
- Moderate Nonproliferative Retinopathy.As the disease progresses, some blood vessels that nourish the retina areblocked.
- Severe Nonproliferative Retinopathy.Many more blood vessels are blocked, depriving several areas of the retina with their blood supply. These areas of the retina send signals to the body to grow new blood vessels fornourishment.
- Proliferative Retinopathy.At this advanced stage, the signals sent by the retina for nourishment trigger the growth of new blood vessels. This condition is called proliferative retinopathy. These new blood vessels are abnormal and fragile. They grow along the retina and along the surface of the clear, vitreous gel that fills the inside of the eye. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls. If they leak blood, severe vision loss and even blindness can result.
Grades of hypertensive retinopathy
Grade 1:Arteriolar constriction/attenuation/sclerosis -silver wiring and vascular tortuosities Grade 2:As grade 1 + Irregularly located, tight constrictions - Known as AV nicking or AV nipping Grade 3:As grade 2 + Retinal edema, cotton wool spots and flame-hemorrhages Grade 4:As grade 3 + swelling of the optic disk (papilloedema) + macular star
