Shortness of breath

History
Presenting complaint
Shortness of breath for ……………..duration

History of the presenting complaint

Describe the onset and progression of the symptom
-Walking distance
-Exercise tolerence
-Interference with day to day activities

• Classify the degree of dyspnoea based on the NYHA classification of dyspnoea

• Describe what has happened to the patient over time

Disease category
Cardiovascular disease
Disease Specific points in the history
Heart failure Congestive heart failure
–Orthopnoea
–Paroxysmal nocturnal Dyspnoea
–Exertional dyspnoea
–Nocturnal cough

Right Ventricular Failure

-Oedema
–Right hypochondrial pain
–Severe Loss of appetite
Ask for a possible aetiology
Past history of ischaemic heart
disease, MI
Past history of valvular (Rheumatic
fever) or congenital heart disease
Family history of cardiomyopathy
Respiratory disease COPD Ask for a history of smoking
(Quantify in pack years), chronic
cough with sputum, history of
recurrent exacerbations(worsening
of shortness of breath with sputum
production)
minimal day to day and day night
variations
ask about inhaler use and response
Bronchial asthma
Intermittent symptoms with diurnal
variation, triggering factors
Family history of atopy and asthma
Childhood history of asthma
Inhaler use
day to day and daynight variations
Diffuse parenchymal lung disease
Non productive cough with minimal
sputum
Progressive shortness of breath
Ask for occupational exposures
Drugs known to cause lung disease
(amiodarone, chemotherapeutic
agents)

Ask for history suggestive of

connective tissue diseases
(SLE, rheumatoid arthritis,
scleroderma) – joint pain, skin
rashes, low grade fever, dry eyes

Pleural effusion (secondary to TB or Ask for history of chronic cough and

bronchial carcinoma)
Hematological disease Anaemia and pancytopenia
hemoptysis, past history of TB,
contact history of TB
Malaise, easy fatigue, site of
bleeding (family history of
anaemia,History of blood
transfusion)

Complications
Heart failure
-Cardiac cirrhosis
-2ry Renal failure
-Arrythmia

Treatment upto now

–Drugs and side effects
–investigations (ECG, Echo, Angiogram, CXR)
-Interventions

Social history
Get a detailed account of the household and occupational environment if you suspect bronchial asthma,

Alcohol ,

Smoking ,

Exercise ,

Lifestyle , income whether can afford surgery / stenting

Examination
General examination

• BMI
• Get a general impression of the patient (Dyspnoeic , Propped UP)
• Cachexia (chronic heart failure, malignancy)
• Examine the skin for any vasculitic rashes (SLE)
• Look for pallor (anaemia)
• Look for peripheral stigmata of hypercholesterolemia (corneal arcus, Tendon xanthoma ,
Xanthalesma)
• Icterus (cardiac cirrhosis in long standing heart failure)
• Cyanosis
• Examine the hands for features of rheumatoid arthritis or scleroderma
• Clubbing (diffuse parenchymal lung disease)
• Ankle oedema
• Look at the surrounding

Cardiovascular system

• Pulse examination
Look for pulsus alternans in severe heart failure Arrhythmias
• JVP – elevated in congestive cardiac failure
• Blood pressure
 • Palpate for a shifted apex (cardiac failure), palpable P2 in cor pulmonale
• Auscultate for murmurs
• Look for fine basal crepts in the lower zones of the lungs (cardiac failure)

Respiratory system

• Examine for the following

• Respiratory rate
• Use of accessory muscle
• COPD , Bronchial asthma – features of hyperinflation
• Pleural effusion
• Pulmonary fibrosis
Abdomen

• Look for a tender pulsatile liver (cardiac failure)

• Ascites (cardiac failure)
Nervous system

• Do a quick examination

Discussion
What are the initial investigations you would like to perform in this patient?
• FBC – to look for anaemia and to look for infection in Bronchial asthma and COPD
• CXR
Look for a respiratory pathology
Look for evidence of cardiac failure Upper lobe diversion
Kerley B lines
Batwing sign
Snow storm appearence
• ECG
Features of ischaemia
Several arrhythmias are known to be associated with heart failure
Poor R wave progression in Heart failure
• Echocardiogram

Assess the ejection fraction

End systolic and end diastolic diameter
Associated valvular abnormalities
Features of Diastolic failure
Segmental wall motion abnormalities
 • Lung function tests if the diagnosis is unclear to look for obstructive or restrictive pulmonary
disease
• Other blood investigations
Renal functions
Serum electrolytes
BNP
LFT

Heart failure
What are the principles of management in a patient with heart failure?
The principles of management of heart failure can be summarized as follows

1.General management
a.Weight reduction
b.Dietary modification
c.ω3 fatty acids
d.Stop smoking
e.Moderate alcohol
f.Regular exercise

2.Pharmacological management
a.Furesemide
b.ACEI
c.β blockers
d.Spirinolactone
e.Digoxin
f.Warfarin if ejection fraction is very low

3.Surgery and interventions

a.Pacemakers
b.Implantable cardiac defibrillator
c.Cardiac resynchronise theraphy
 The following drugs are used in the management
Class Drugs Side effects Special points
Diuretics Frusemide Postural hypotension Check renal function and
Metabolic disturbances electrolyte imbalances prior
Hyperglycaemia to commencement of
Hyperuricaemia therapy
Hypokalemia
Hyponatremia Start at a low dose and
Other monitor the weight
Urinary retention
ACEI Captopril Dry cough Are 1st line drugs in the
Enalapril 1st dose hypotension management of heart failure
Postural hypotension 1st dose should be given as a
Electrolyte imbalances – low dose before the patient
hyperkalemia Angioedema sleeps
Do renal functions and SE
before commencing
Contraindications
Significant renal dysfunction
Hyperkalemia
Bilateral renal artery stenosis
Severe aortic stenosis

Angiotensin II receptor Losartan Are used when the patient

blockers cannot tolerate ACEI
Beta blockers Bisoprolol Bradycardia, conduction Is contraindicated in patients
Metoprolol abnormalities, with asthma, significant
bronchoconstriction, heart block
worsening of peripheral
vascular disease, impotence

Aldosterone antagonists Spiranolactone Painful gynaecomastia Take care when using as

Hyperkalemia combination therapy
Cardiac glycosides Digoxin Heart block May be considered as
Pre excitation syndromes second line therapy in heart
failure
COPD
History
Important factors

Smoking
Occupational exposure
Progressive SOB
History of exacerbations
Inhaler use, Response to inhalers
Minimal day to day and day night variations

Physical signs
Usually late
Thin wasted person
Hyperinflation of chest
B/L Rhonchi on auscultation
Cyanosis and Polycythaemia
Cor pulmonale

Diagnosis
 FEV1 < 80% Predicted
 FEV1/ FVC ratio < 70%
 Poorly reversible with bronchodilators
 Increased TLC, FRC, RV
 Reduced DLCO

MANAGEMENT
Pulmonary rehabilitation – Education and training program to help patient to live an active life within
the limitation of symptoms
 Stopping smoking
 Controlling breathlessness
o Breathing control
o Pursed lip breathing
o Correct posture
 Clearing sputum from the lungs
 Daily activities made easier
 Exercise, sleep, diet
 Psychological support

COMPLICATIONS
 recurrent exacerbations by URTI,
 co-pulmonale,
 type II respiratory failure,
 pneumothorax,
 polycythaemia
 systemic effects (muscle wasting,
muscle fatigue
Bronchial asthma
Presenting complain

Cough
Wheezing
Shortness of breath
Chest tightness
Age of onset
Precipitating factors
Progression
History of acute exacerbations

Treatment (which has been given so far)

Long term prophylaxis

Method of administration
Compliance & Techniques

Side effects of drugs

–Tremors
–Palpitations
–increased Weight gain

Day time activity

Night time disturbance
Other atopic conditions Allergic rhinitis
- Allergic conjuntivitis
- Eczema
- Urticaria and angioedema
- Food and drug allergies

Birth history
Dietary history( food avoided)
Family history (BA and Atophy)

Social history

Impact on the patient

Impact on the family
Environment
Knowledge about the disease
Indications for reliever medications in bronchial asthma

• Chronic persistent asthma

• After an episode of life threatening asthma
• Recent increase in the severity or frequency of acute exacerbations
• Nocturnal asthma which disturbs the child from sleep
 • Frequent episodic asthma which interferes with normal life
• Severe exercise induced asthma
• Inaccessibility of medical care

Regular assessment and follow up

The following should be assessed at a routine asthma follow up

• Signs and symptoms of asthma

• Pulmonary function
• Quality of life and functional status
• Acute exacerbations during this period
Adequacy of the management
Pharmacotherapy
Consider step up or step down every 3 months
Environmental modifications
• Assess for the side effects of the medication – especially steroids
Assessment of the weight and height
Measure the blood pressure
Encourage exercise
Adequate dietary calcium supplementation Ophthalmological
assessment
Central chest pain

Presenting complaint
• Chest pain – This is usually of acute onset

History of the presenting complaint

1. symptom analysis
Ch – Character
L – Location
O- Onset
R- Radiation (Jaw, Shoulder , Medial border of left upper limb)
I- Intensity
D- Duration
E- Exacerbating factors , Relieving factors
Associated autonomic features
–Sweating
– Nausea
-Vomiting

2.Differential Diagnosis /Aetiology

Condition History
ACS • Acute onset central chest pain, Tightening in nature
• Radiating along the left arm and to the jaw
• Lasts for more than 30 minutes
• Associated with autonomic symptoms such as sweating
• Not relived by rest or GTN. Risk factors +
Aortic dissection • Sudden onset tearing chest pain radiating to the interscapular
region.
• Pain is usually maximal at the onset
• Risk factors – HT, Marfan syndrome
Acute • Central chest pain
percarditis • Referred to neck arm or left shoulder
• Increased with inspiration and lying supine
• Decreased on bending forwards

PE • Associated SOB and hemoptysis

• Pleuritic type chest pain
• Risk factors for DVT
Pneumothorax Usually causes peripheral chest pain

Oesophageal Past history of dyspeptic symptoms

pain
Peptic ulcer Past history of dyspeptic symptoms, acute abdominal pain,
disease hematemesis and malaena

Acute Associated epigastric pain radiating through the back,

pancreatitis relieved with the patient bending forwards

3.Complications
– Heart failure
- Arrythmia

4.Treatment upto now

…………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………...

Past medical history

• Previous episodes of chest pain
• Past history of diabetes mellitus, hypertension, hyperlipidaemia
• Always remember to take a detailed history of each of the above co morbidities if they are
present
• Ask for any other significant co morbidities
• Ask for smoking and use of alcohol

Family history
• Ask for a family history of young onset IHD, DM, hypertension, hyperlipidaemia
Social history

–Smoking
–Alcohol
–Lifestyle
–Exercise
–Diet
–Knowledge

Examination
General examination

• Get a general impression of the patient -ill looking ,Sweaty ,

• BMI – Abdominal circumference
• Look for features of Marfan’s syndrome – can present with aortic dissection)
• Look for peripheral signs of hypercholesterolemia (Xanthelasma, corneal arcus)
• Pallor (Can aggravate ischaemic heart disease)
• Examine the fundi (Hypertensive , Diabetic eye changes)
• Examine the limbs for features of DVT (pulmonary embolism)
• Look for ankle edema
CVS

• Measure the blood pressure – remember to measure this in both hands (can differ in aortic
dissection)
• Examine the pulse for bradycardia (heart block associated with MI and Arrythmias)
• Look for features of cardiac failure – cardiac dilation, S3, gallop rhythm
• Look for a pericardial rub (acute pericarditis) Examine for murmurs
MR – Acute MI due to rupture of papillary muscles
VSD – Complication of MI
AR – Aortic dissection
• Loud P2 – pulmonary embolism
RS

• Examine for bi basal crepitations – heart failure

• Exclude any respiratory pathology – especially a pneumothorax
Abdomen

• Palpate the abdomen – especially in the epigastrium and right hypochondrium for
tenderness
 Acute management
• Admit the patient
• Give a bed close to the nurses’ station
• Check A, B, C and correct as necessary. Administer oxygen
• Connect to a cardiac monitor if available
• After initial resuscitation take a quick history and do a targeted clinical examination with 3
objectives in mind
 Exclude differential diagnosis
 Look for associated complications
 Co morbidities which will directly affect the management
Look for complications
• Cardiac failure
• Arrhythmias
• After making a clinical diagnosis of MI based on the history and examination it is important
to proceed with investigations
• Blood – FBC, SE, BU, SC, lipid profile, cardiac biomarkers(Troponin I), blood sugar

• Arrange for an inward 12 lead ECG and inward CXR if suspecting cardiac failure
• Interpret the ECG
ST elevations – STEMI No ST elevations but ST depressions and T inversions – Unstable angina
or NSTEMI and new onset LBBB

ECG changes associated with a STEMI?

Time Changes
Hyperacute (0-20 min) Tall peaking T waves and progressive ST elevations
Acute (min – hours) ST elevations
Early (hours – days) ST elevations disappear and Q waves appear
Indeterminate (days – weeks) Q waves and T inversions
Old Persistence of ST elevations

Anterior –V3-V5
Anteroseptal –V1-V3
Lateral –V4-V6,aVL,L1
Inferior L2,L3,AVF
R/ Ventricle –V4R
• Commence drug therapy – Aspirin 300mg oral (chewed), clopidogrel 300mg, morphine 2.5-
5mg IV and metaclopramide 10mg IV. Consider administering nitrates after exclusion of
hypotension.
• Commence strategies to limit infarct size
• Beta blockers (CI in patients with HR<60, SBP <100, conduction defects and history of asthma
 • ACEI
• Statin
• Reperfusion
• Heparin (LMWH)

Unstable angina
Acute coronary LMWH
syndrome NSTEMI Iry PCI
STEMI
LBBB Streptokinase

• Reperfusion is available as 2 options. One is drug based thrombolysis and the other is
percutaneous coronary intervention (PCI). However PCI is not routinely available in the
government sector in SL.
The decision for thrombolysis is made based on the clinical history and the ECG findings.

What are the indications for thrombolysis?

• Within 12 hours of onset of pain
• ECG evidence of ST elevation
• New onset LBBB

• True posterior MI

If the decision is made to use thrombolysis the CI should be excluded

Absolute contraindications for thrombolysis

• Past history of a hemorrhagic stroke

• Past history of an ischaemic stroke within the last 6 months
• Intracranial tumor
• Aortic dissection
• Active internal bleeding within the last 2 weeks

1.5 million units of Streptokinase in 100ml of N/Saline infusion over 1 Hour

 More allergic reactions

 Patient should be in a monitoring bed with a cardiac monitor
Compare thrombolysis to primary PCI in the management of acute STEMI
• In Sri Lanka primary PCI facilities are extremely limited and most patients will receive
thrombolysis
• However PCI should be considered in patients who have contraindications for thrombolysis
or have STEMI complicated with cardiogenic shock

How would you assess the response to thrombolysis?

• Relief of pain
• Restoration of hemodynamic stability
• Reduction of ST elevations by 50% in 60-90 minutes following administration (Remember
that persistent ST elevations could indicate a left ventricular aneurysm)

Subsequent management
• Ask how the patient feels and establish the symptoms
• Examine the patient to look for complications (see below)
• Order the necessary investigations
• Look in to the management – look at the drugs the patient is receiving Antiplatelet drugs –
Aspirin and clopidogrel (now on maintenance doses)
Nitrates - ISDN
Beta blockers
ACEI
Statins
• Initiate or modify the management of co morbidities – DM, hypertension
• Look into the risk factors and start a program of cardiac rehabilitation and risk factor
modification

• What are the complications of an acute STEMI? State the

principles of management
Timing Complication Management
Early Arrhythmias VF – Immediate cardioversion
Manage other arrhythmias
Heart block Use atropine
Consider temporary cardiac
pacing
Heart failure and cardiogenic Manage heart failure Use
shock inotropes in the
management of cardiogenic
shock
Post infarction angina Increase the dose of the anti
anginal drugs. Consider coronary
angiography
Acute pericarditis Usually no treatment required
Acute MR Refer for surgical repair
Intermediate and late VSD
 Dressler’s syndrome

What are the principles of management of the patient prior to discharge?

• Counsel the patient regarding lifestyle modifications
• Discuss the management of stress
• Perform a risk stratification and plan for further investigations
Echocardiography to assess the left ventricular function
Plan stress testing if required by the consultant
Coronary angiography
• Discharge medications
• Cardiac rehabilitation and reintegration to the patient’s day to day activities

Management of a patient with UA/NSTEMI

• The initial management of the patient should take place as described above
• Diagnosis is based on the ECG and cardiac biomarkers
Patients with unstable angina/NSTEMI present with acute chest pain
ECG may show ST depressions and T inversions
Cardiac biomarkers are positive in NSTEMI and negative in UA
• Heparin should be administered in these patients – LMWH
• There is no place for the use of thrombolytics in patients with UA/NSTEMI
• Other principles of management are the same as in STEMI
Generalized oedema

Presenting complaint
The patient presents with generalised body swelling for ……………. duration

History of the presenting complaint

Symptom analysis

1. Onset (gradual or sudden)

2. Describe the distribution of oedema whether is predominantly ascites or generalised oedema

3. Diurnal variation
–Heart failure- predominantly evening
–Renal – predominantly – morning

Cause Specific points in the history

CVS
Heart failure Exertional dyspnoea
Paroxysmal nocturnal dyspnoea LVF
Orthopnoea
Ankle oedema worse in evening
liver congestion – RHC pain RVF
Intestinal congestion – Severe loss of appetite
Ask about aetiology – ischaemic heart failure,
Valvular heart disease , Cardiomyopathy

RS
Cor pulmonale Ask for a past history of chronic cough and sputum
production (COPD) smoking
GIT
Chronic liver disease Abdominal distension > Ankle oedema
Jaundice

See for other complications

a. Portal hypertension – Haematemesis , Malaena
b. Hepatic encephalopathy
–Altered behaviors
-Day night reversal
-Confusion
c. Bleeding manifestation
d. Hepatorenal syndrome
– decreased UOP
- uraemic features
e. Hyperpigmentation
f. Spontaneous bacterial peritonitis
– worsening of ascites
– Abdominal pain
- Fever
g. Endocrine complications
– Hypoglycaemia
– Hypogonadism (impotence, loss of libido)

Ask questions for a probable aetiology

-Alcohol intake
-Sexual promiscuity, intravenous drug use (Hep B)
-Ayurvedic or long term drug use
-Joint pain, skin rashes, history of autoimmune
disease (Autoimmune hepatitis)
-Movement disorders (Wilson’s disease)
-Family history of liver disease,
-Biliary disease

Renal disease
Glomerulonephritis -Oedema mainly in evening
– Periorbital oedema , Generalised odema
– Froth in urine
– Haematuria
– Decrease in UOP
Probable aetiology
Ask for evidence of an autoimmune disease Skin
rashes, joint pain, fever and other evidence of
systemic involvement
Hep B
Lymphoma
Malaria
Drugs ,DM
 Complications of nephrotic xd
- DVT
-Hypovolaemia
-CKD

Chronic kidney disease

-Decrease in urine output
– Uraemic features
– Risk factors (DM , Hyper tension)

Endocrine disease Ask for symptoms of hypothyroidism

Malabsorption Steatorrhoea , weight loss, Anaemic features

Complications ----

Treatment upto now

-No of hospital admissions
-UGIE and bandings
-Blood transfusion
- Possibility of liver transplantation

PMHx –
PSHx –

All hx –
Social Hx –
Alcohol – CAGE questionaire
C- Cut down
A – Annoyed
G – Guilty
E- Eye opener

Monthly income , Family support , Social services available , Social relationships

Examination
General examination

• General condition of the patient

• Pallor
• Icterus (Liver disease)
 • Peripheral stigmata of chronic liver disease – parotid swelling, palmar erythema, dupuytren
contractures, gynaecomastia, spider naevi
• Clubbing
• Flapping tremors
• Vasculitic rashes
• Lack of axillary and pubic hair
• Testicular atrophy
• Injection sites , Hyper pigmentation
• Oedema
• Hands – Leuconychia , Hepatic flaps , clubbing
Abdominal examination

Gross distension
Caput medusa
Dilated veins
Sighns of peritoneal irritation
Hepatomegaly
Splenomegaly
Ascites
Hepatic bruit (alcoholic hepatitis HCC)
Respiratory system

• Pleural effusion
Cardiovascular system

• Look for evidence of cardiac failure

• Co pulmonale

Summary

………………………………………………………………………………………………………………………………………………………
……………………………………………………………………………………………………………………………………………………
……………………………………………………………………………………………………………………………………………………
……………………………………………………………………………………………………………………………………………………
……………………………………………………………………………………………………………………………………………………

Problem list

-Decompensated / compensated liver disease

– Aetiology
– Complications
– Social problems or economical problems
Investigations
Severity and complications

 Liver function -Serum albumin reduced/ reversed albumin globulin ratio

–PT/INR- Prolonged
 Liver biochemistry
-Depends on the severity
– Decompensated disease
– ALP
– ALT &AST b
-ALT/AST ratio is reversed in established Cirrhosis, Alcoholic hepatitis or Denque hepatitis

 FBC : Platelet count ( due to hypersplenism)/pancytopenia

 Serum electrolytes
Low sodium indicates severe liver disease due to a defect in free water clearence or excess
diuretic theraphy
 Serum createnine An elevated concentration >130µmol/l is a marker of worse prognosis
 OGD – to detect evidence of portal hypertension-Osophageal varices/portal gastropathy

To detect aetiology / type

 Serum α feto protein

If > 400mg/ml is strongly suggestive of the presence of hepatocellular carcinoma
 Serum auto antibodies – Autoimmune hepatitis
 Viral markers – Viral hepatitis
 Serum immunoglobulins - Viral hepatitis
 Iron indices (TIBC) & S.Ferritin- Herediary haemochromatosis
 24 hour urine copper & ceruloplasmin levels (Wilson’s disease)
 Antitrypsin levels – Cystic fibrosis

Imaging (USS/CT/MRI)

USS

o changes in the size and shape of liver

o Fatty change & fibrosis produce a diffuse increased echogenicity
o In established cirrhosis there may be marginal nodularity of the liver surface and
distortion of the arterial vascular architecture
o The patency of the portal and hepatic veins can be evaluated
o Useful in detecting hepatocellular carcinoma
o Elastography is being used in diagnosis and follow up to avoid liver biopsy

 Liver biopsy
 MANAGEMENT
Overview

1. Treat /avoid cause if possible

a. Abstain from alcohol

b. Anti viral drugs for HBV
c. Venesection for Haematemesis
d. Penicillamine for Wilson’s disease

2. Treat decompensation

a. Liver failure
b. Portal hypertension

3. Detect or prevent complication and follow up

a. Clinical presentation
b. LFT, PT, FBC, Creatinine and electrolytes
c. USS abdomen & α feto protein
d. OGD in 12 months

4. Liver transplantation

Cirrhosis

• General management
• Remove or treat causative agent, if possible
• Especially important in alcohol, HBV, HCV, Wilson disease, hemochromatosis
• Adequate diet
• Correct deficiencies of protein, calorie, vitamins, minerals
• Vegetable protein: 1 g/kg/day ( decreased aromatic aminoacid) (Hepatic
encephalopathy- decreased branched chain aa, increased aromatic aa)
• Adequate calorie intake to prevent proteolysis: 25-35 kcal/kg/day
• Vitamin+mineral supplementation
• Salt restriction
• Avoid physical exertion, dehydration
• Vaccines: HAV, HBV, pneumococcal vaccine, annual ‘flu vaccine
• Avoid precipitating factors of hepatic encephalopathy
Dehydration, constipation, hypokalemia, hyponatremia, drugs, infection, surgery, upper GI
bleeding, hypovolemia
 Management of complications

Management of haematemesis

 Initial resuscitation
 Place the patient in the left lateral position to prevent aspiration of blood
 Insert 2 wide bore IV cannulae
 Collect blood for investigations especially full blood count and grouping and DT
 Give IV 0.9% saline bolus as initial volume resuscitation – 20ml/kg
 Consider giving FFP and packed cells
 IV omeprazole
 IV vasopression or IV octreotide ( CI- IHD) Terlipressin – decreases mortality
 Start prophylactic antibiotics- 3rd generation cephalosporin
 Urgent endoscopic treatment is the treatment of choice but it is not readily available in Sri
Lanka- injection sclerotheray or banding

Other options of management

 Ballontamponade with a Sengstaken- Blakemore tube

Further Management
 Give drugs used in the management of hepatic enceophalopqathy
 Consider prophylaxis with oral propranolol- non selective beta blockade- decreased cardiac
output, blockade of beta 2 vasodilator properties
 Follow up endoscopy- repeat endoscopy, TIPS-increased risk encephalopathy

Treatment of ascites
Start input output chart and daily weight chart
Salt-restricted diet (<2 g/d)
Diuretics
Check creatinine and electrolytes before commencement
Furosemide + spironolactone combination (ratio 40mg : 100mg), once daily
Increase doses once in 3-5 days, until weight loss 0.5 kg/d or maximum doses
(160/400) reached
Watch for electrolyte imbalance
Large-volume paracentesis
Not done if electrolyte imbalance, cardiac or renal impairment present
5 L/d
With or without IV albumin (controversial), 10 g/1L
Watch out for hepatic encephalopathy and pre-renal ARF

Treatment of spontaneous bacterial peritonitis

• Must be differentiated from

• secondary bacterial peritonitis
• and other causes of worsening ascites, such as tuberculosis, malignancy,
acute pancreatitis
 • Empirical broad-spectrum antibiotics
• To cover aerobic enteric flora and pneumococci
• IV ceftriaxone or ciprofloxacin →oral coamoxiclav or cirpofloxacin (total 5
days)
• Consider secondary prophylaxis with norfloxacin (400 mg/d) or
cotrimoxazole (2 tabs/d, 5 times a week)
• IV albumin reduces mortality
• 1.5 g/kg initially, 1 g/kg 48h later
• Look for adrenal insufficiency and correct it

Management of hepatic encephalopathy in a patient with cirrhosis

 Minimal normal standard clinical exam abnormal responses to detailed

psychometric
 Tests
 Stage 1: mild confusion, reversed sleep-wake cycle, irritability, reduced
attention span
 Stage 2: slurred speech, drowsiness, lethargy, intermittent disorientation,
asterixis
 Stage 3: gross disorientation, somnolent but arousable, hyper-reflexia
 Stage 4: stupor or coma

Precipitating factors
Gastrointestinal- haemorrhage, constipation, high protein diet
Infection-SBP,pneumonia, UTI
Electrolyte imbalances- hypokalemia, dehydration, uraemia
Drugs- benzodiazepines, sedatives, potassium losing diuretics
Clinical features- change in personality
reversal of sleep pattern
confusion
disorientation,
hyper reflexia and increased tone
fetor hepaticus
constructional apraxia
decreased mental function
EEG- decreaed α to delta ratio

Initial management
Grade
Elevate the head end
Input/output chart and proper fluid management
Nutrition – protein can be withdrawn in first 2-3 days nutrition 25-35 kcal/kg/day and
protein intake 0.5-1.2 g/kg/day should be maintained
Maintain electrolyte balance
Treat infection
Reduce N load from gut
-lactulose
-metranidazole 200 mg tds
Branched aminoacid –LOLA
Mannitol should be considered in patients with cerebral oedema
Chronic renal failure

History
Presenting complaint
Shortness of breath
Generalised body swelling or periorbital swelling Exclude other aetiologies
Decreased UOP

History Presenting complaint

Symptom analysis

1. Urine output

Features of fluid overload

SOB
2. Orthopnoea
Ankle oedema
3. Uraemic features
Malaise
Lethargy
LOA
Itching
Nausea, vomiting, diarrhoea

• Describe the initial diagnosis of chronic renal failure

• Presenting symptoms of the patient, initial investigations performed and their results
Probable aetiology of the disease

• Diabetes mellitus
• Hypertension
• Past hx of UTI / Pyelonephritis
• Family history of kidney disease – PCKD
• Glomerulonephritis
Ask for preceding/ childhood history of edema, frothy urine and hematuria
Ask for any symptoms of autoimmune disease – rashes, joint pain, malaise, low grade fever
History of diabetes mellitus
• Vascular disease – Preceding hypertension
• Tubulointerstitial diseases – Long term use of drugs
• Obstructive uropathy – Preceding symptoms of LUTS, calculus disease
• History of snake bite
Complications- Pulmonary oedema
- Acute pericarditis
 -Anaemia
-Renal osteodystrophy
-Nervous system complications
- Hypocalcemia

Treatment upto now

When was it diagnosed
How was it diagnosed
Results about Renal function tests
Any haemodialysis done
Freguency of haemodialysis
Arterio venous fistula creation
Plan for transplant
Availability of donor
Management of anaemia - EPO injection , Blood transfusion
Renal biopsy
Current medications

Past medical history

DM , HT , SLE
Establish the other co morbidities and describe them

Social history
• Discuss the impact of the disease on the patient’s life
• Family support for the patient
• Access to dialysis

• Distance to hospital

Examination
General examination

• Conscious level
• Pallor
• Brownish discolouration of the nails
• Arteriovenous fistula (functional or not)
• Flapping tremors
• Scratch marks on the skin, pigmentation, bruising
 • Ankle oedema
• Any neck or femoral line
CVS

• Measure the blood pressure

• Look at the JVP
• Pericardial friction rub
• Look for signs of heart failure
• Flow murmurs

RS

• Pleural effusion
Abdomen

• Palpable renal masses (PCKD)

Ascites

CNS

Features of peripheral neuropathy

Discussion
Stages of CKD?

Treatment
 Stage 1/2/3/4/5
o Measures to retard disease progression
 Stage 3/4/5
o Measures to reduce symptoms
 Stage 5
o Renal replacement therapy

Measures to retard progression

 Reduce Intra renal BP
 Reduce Systemic BP
 Reduce RAS pathway activation
 Block AT/aldosterone/PGE2….TGF beta
 Reduce Proteinura
 Reduce Cytokine release
One single intervention alone is not enough
A multiple risk modification is required
Intervention must be early for maximum benefit

Measures for symptomatic management

 Furosemide
 Nifedipine
 Domperidone
 1 alpha calcidol
 Erythropoietin
 Emollient ointment
 Calcium carbonate
 Sodium bicarbonate powder
 Polystyrene resins
Measures for renal replacement therapy
 Dialysis
o Haemo-dialysis
o Peritoneal-dialysis
 Transplant
o Cadaveric
o Live
 Related
 Non-related

Anaemia of Renal disease

 Multifactorial
o Loss of appetite
o Blood loss from GIT
o Erythropoietin deficiency
 Treatment involves
o Look at blood picture
o Assess iron stores/folate/B 12
Erythropoietin replacement ± Fe/ Folate/ B12
Nephrotic syndrome
History
Presenting complain - Oedema Generalised

Partial

Froth in the urine

Urine home test positive

Hx of presenting complain :
onset
Distribution
Progression : periorbital limbs abdomen

Scrotal oedema

Association ; Froth in the urine

Haematuria
Reduced UOP
Dysuria

Complications

Hypovolaemia – Reduced UOP , Abdominal pain

Pleural effusion

Spontaneous bacterial peritonitis (Abdominal pain)

Thrombosis : renal vein thrombosis (Haematuria , Abdominal pain)

Infections

Past episode

First episode – How long treated

Drugs used

No of relapses

When did the patient relapse? While on steroids or during remission

Side effects of steroids –

Paediatrics – Vaccination history

Social history :
What is the definition of nephrotic syndrome?
• Generalized oedema
• Overt proteinuria > 3.5g/24h
• Hypoalbuminaemia (< 30 g/L)
• Hyperlipidaemia

Frinciples of management of nephrotic syndrome

Find a cause/ underlying pathology

• Assess for a secondary cause based on the history and examination

Consider performing a renal biopsy

Definitive management depends on the cause

Supportive management

• Start monitoring the patient with a daily weight chart and an input output chart
• Recommend a low salt diet for the patient
• Start diuretics for the edema. Carefully monitor the renal functions and electrolytes
• ACEI to control proteinuria
• Consider starting lipid lowering drugs for the hypercholesterolemia
• Monitor for complications
Venous thromboembolism – consider prophylactic anticoagulation if patient
immobilized Infection

• Definitive treatment - Steroids

- Immunosuppressive treatment
- Renal transplant
Jaundice

History
Presenting complaint
• Yellowish discolouration of the eyes for ……… duration

History of the presenting complaint

• Describe the onset and progression of the symptoms in detail
o When was it first diagnosed
o How was it diagnosed
o Was it intermittent or progressive
o How was the progression
o What is the urine colour
o What is the stool colour
o Is there any pruritus
o Are there any anaemic symptoms

• The next step is to differentiate the three main clinical syndromes of jaundice
Pre hepatic Hepatic Post hepatic (cholestatic)
o Is usually due to Mixture of both prehepatic and Presents with dark urine and
hemolytic anaemia post hepatic pale stools
-Deep jaundice There is usually associated
o Very mild jaundice usually -Dark urine pruritus
noticed by someone else -Dark stool
o Presents with dark colour
urine and dark colour
stools
o Associated features of
anaemia are present
(Lethargy / Malaise)

The 2 important cases of jaundice are

• Jaundice with anaemia

• Cholestatic jaundice ( Medicine – Intrahepatic cholestasis)
Jaundice with features of anaemia
• Think of a differential diagnosis and ask direct questions

Cause Specific questions in the history

Congenital hemolytic anaemia Ask for past history of neonatal jaundice
(Age of onset childhood) Recurrent blood transfusions due to symptomatic
anaemia
1.Membrane defects Family history of hemolytic anaemia
2.Enzyme defect
Specific features of individual hemolytic
anaemias
Hereditary spherocytosis
History of leg ulcers
Episodes of aplastic anaemia (Ask for features
of pancytopenia)
Sickle cell anaemia
Leg ulcers
Past history of episodes of sickle crisis
Bone pain and pain in the extremities
Aplasia
Episodes of respiratory distress
Neurological symptoms - stroke

G6PD deficiency
Triggering of episodes of jaundice due to drugs
and certain food items
Jaundice intermittened but non progressive
Complications
History suggestive of biliary colic (Gall stone
disease)
Features of iron overload
Acquired hemolytic anaemia Febrile illness
Warm autoimmune hemolytic anaemia Ask for history suggestive of autoimmune diseases
SLE
Joint pain, alopecia, oral ulcers, Skin rashes
Hematological malignancy
LOA, LOW, neck lumps
Drug history
Treatment with steroids

Ask for pain and bluish discolouration of the

Cold autoimmune hemolytic anaemia peripheries When exposed to cold

Ask for history of preceding respiratory tract

infection - Mycoplasma infection

Passage of dark coloured urine in the night and

Non immune hemolytic anaemia early morning (PNH) - Also can get Thrombosis
(Esp: Budd Chiari syndrome)

History of prosthetic valve surgery

(Mechanical hemolysis)
Associated systemic illness and bleeding
manifestations (DIC)

Complications of haemolytic anaemia

o Heart failure – Shortness of breath, Orthopnoea ,Exertional dyspnoea

o Gallstones – RHC pain / Biliary colic and Dyspeptic symptom
o Complications of blood transfusions
-Blood borne infections
-Reaction to transfusion
-Iron overload

Complete the other components of the history

Social history
• Get a detailed social history if the patient has a chronic hemolytic anaemia
• Disease impact on the patient
• Disease impact on the family
• Family support

Pre Hepatic Jaundice

Examination
General examination

• Pallor
• Icterus – Mild tinge in haemolytic anaemia , Deep jaundice in Cholestasis
• Lymphadenopathy
• Skin rashes – especially vasculitic rashes (warm autoimmune hemolytic anaemia)
• Thalassemic facies
• Leg ulcers (sickle cell anaemia)

Abdomen
• Hepatosplenomegaly

Cardiovascular :Look for features of heart failure due to anaemia

Discussion
Investigations in suspected Haemolytic anaemia
1.FBC with red cell indices and Reticulocyte count , Blood picture

Category Cause Blood film Other investigations

Congenital Hereditary spherocytosis Spherocytes

G6PD deficiency Bite cells, blister cells, G6PD levels

polychromasia due to
increased reticulocytes
Special stain demonstrates
Heinz bodies

Thalassemia Microcytic hypochromic Hb electrophoresis

cells, abundant target cells,
nucleated RBCs, basophilic
stippling
Sickle cell anaemia Sickle cells Hb electrophoresis
Acquired Warm autoimmune Spherocytes Positive Coombs
hemolytic anemia test
ANA
Cold Cold agglutinin test

2.Investigations showing evidence of hemolysis

• Total bilirubin with Direct and Indirect fractions

• Increased unconjugated bilirubin
• Increased LDH
• Increased reticulocyte count
• Urinary haemosiderin (evidence of intravascular hemolysis)
• Urine urobilinogen – increased in haemolytic jaundice but not in other prehepatic type
• Perform a blood film

3.Coombs test to see immune or non immune

4. Liver Function test

Management –Management of individual haemolytic anaemias

Cholestatic jaundice
-Intrahepatic Cholestasis
–Extrahepatic Cholestasis

Presenting complaint
Deep yellow discoloration of eyes for …………duration

History of the presenting complaint

Associated features

o Dark colour urine

o Pale stools
o Pruritus

Intrahepatic cholestasis

Cause Specific points in the history

Infective
Viral hepatitis (esp Hepatitis A) Ask for preceding prodromal illness – headache,
arthralgia, myalgia, nausea and anorexia

Ask for risk factors

Consumption of unhygienic food and water
After few days develop jaundice

Sexual promiscuity, use of IV drugs and past

history of blood transfusions
Inflammatory Female , Middle age , Joint pain , Skin rash and hair
Autoimmune hepatitis loss
Ask for past history of other autoimmune diseases
Primary biliary cirrhosis
Preceding history of fatigue and pruritus
Associated joint pain and early morning stiffness
suggestive of an inflammatory arthropathy
Metabolic
 Alcoholic hepatitis Ask for history of alcohol ingestion

 NASH DM , Obesity , Hyperlipidaemia

 Drugs Obtain a detailed drug history

Ask for the use of ayurvedic/ herbal preparations
 Wilson’s disease Especially young age/ Tremor , Family history
  Haemochromatosis Hyper pigmentation
New onset DM
Cardiomyopathy

Malignancies
Primary and secondary liver malignancies Ask for past history of malignancies
Symptoms suggestive of primary malignancies-
GIT, breast

Ask for associated LOA and LOW

Extrahepatic cholestasis
 Complications
o Steatorrhoea
o Fat soluble vitamin deficiencies (A,D,E,K)
-Especially bleeding manifestations
o Cholangitis – If extrahepatic Cholestasis
o Hepatorenal syndrome - Reduced UOP , Uraemic features

Treatment upto now

Investigations – USS , CECT , ERCP/MRCP

Complete the other components of the history

Examination
General examination

• General examination is extremely important. Look for

Icterus - Deep
Pallor
Features of chronic liver disease
Xanthelasma (Primary biliary cirrhosis)
Injection sites (Hepatitis B)
Rashes (SLE – autoimmune hepatitis)
Lymphadenopathy – especially for left supraclavicular lymphadenopathy
Skin – scratch marks, bleeding manifestations
• Abdominal examination
Do a routine abdominal examination. The most important point is to look for a palpable gall
bladder
Courvoisier’s law states that if the patient with obstructive jaundice has a palpable gall
bladder the cause for the jaundice is unlikely to be due to gall stones

Discussion
How would you investigate a patient with cholestatic jaundice?
• Total bilirubin with direct fraction – Total bilirubin will be elevated with increased direct
fraction
• Urinary urobilinogen
• Liver function tests – The typical pattern will be elevation of alkaline phosphatase and GGT
out of proportion to the rise in transaminases
• Imaging studies – Ultrasound scan of the abdomen is an extremely important investigation
in the basic assessment of a patient with obstructive jaundice. Look for the dilation of the
intrahepatic and extrahepatic duct system. The diameter of the normal common bile duct is
less than 6mm
Dilation of both IH and EH ducts
Pancreatic head mass
Stone in the common bile duct
Only IH duct dilation No duct dilation
Hilar cholangiocarcinoma Medical (Intrahepatic
Gallbladder pathology cholestasis)
Mirizzi’s syndrome
Porta hepatis lymphadenopathy

Further investigation of cholestasis without duct dilation

• Hepatitis serology
• ANA and serum immunoglobulin (Autoimmune hepatitis)
• Anti- smooth muscle antibodies (Primary biliary cirrhosis)

The final set of investigations are carried out to investigate for the complications of cholestatic
jaundice

• PT/INR – To look for coagulopathy

• Renal function tests – To look for Hepatorenal syndrome
Stroke

History
Presenting complaint
Sudden onset

• Face , Arm , Leg weakness

• Altered consciousness

• Facial weakness , double vision , Facial numbness

• Difficulty in talking , Dysphagia , nasal regurgitation

• Loss of balance / Ataxia (Cerebellar)

The patient will have presented with a focal or global (loss of consciousness) neurological
deficit

State the duration

History of the presenting complaint

Describe the symptoms the patient experienced

Symptom analysis
1. What was he doing at the time of stroke
2. Type of weakness (Face / Arm / Leg / Speech)
3. Loss of consciousness
4. Predominant upper limb or lower limb involvement
5. Progression of symptoms
- Disappearance
- Static
- Worsening
5.Associated symptoms
- Severe Headache
- Vomiting
- Seizures
Next try to establish the clinical pattern of stroke

Type of stroke Symptoms

Anterior circulation Face arm and leg weakness

Ask for evidence of higher cortical dysfunction
Language and speech
Memory
Calculation and making decisions
Posterior circulation Ask for associated
Diplopia
Vertigo
Facial numbness and weakness
Dysphagia and nasal regurgitation
Slurring of speech
Imbalance and unsteadiness
Lacunar circulation No specific symptoms

Ask for other associated neurological features

• Bladder and bowel incontinence

Determine the aetiology of the stroke

Ischaemic

Cause Specific points in the history

Atherosclerosis Ask for past history of DM, HT and ischaemic heart

disease
Smoking, hyperlipidaemia
Ask for symptoms suggestive of atherosclerosis
Chest pain – angina
Intermittent claudication – PVD
Past history of TIA
Cardioembolism Past history of rheumatic fever and valvular heart
disease
History of MI (intramural thrombus)
History of palpitations and syncope (arrhythmias)
History suggestive if infective endocarditis
Vasculitis Infective
Sexual promiscuity, blood transfusions, use of IV
drugs (syphilis and HIV)

Autoimmune disease
Ask for joint pain, skin rashes, oral ulcers, hair loss,
hematuria
Long standing low grade fever and malaise
Thrombophilias Ask for family history of young stroke, recurrent
pregnancy losses

Exclude other stroke like events

• Exclude a history of trauma

• Ask for a preceding history of early morning headache with associated vomiting (tumor)
• Ask for a history of unilateral throbbing type headache prior to the event with preceding
aura (hemiplegic migraine)
• Ask for abnormal movements preceding the weakness and past history of seizures (post
ictal Todd’s paresis)
• Ask for any fever and altered behavior before the event (CNS infection)
• Ask for symptoms of hypoglycaemia and any past history of liver or renal disease (metabolic
encephalopathy)
• Ask for recreational drug use

Hemorrhagic stroke

Ask for use of anticoagulants

Complications

• Medical – Infections such as respiratory tract infections and UTI

• Associated neurological problems - seizures
• Pressure sores
• DVT
• Describe the psychological state of the patient
Level of functioning of the patient - Barthel index

Finally the most important is to describe the level of functioning of the patient. Describe the
following details on the patient

• Bathing
• Use of the toilet
• Dressing
• Personal hygiene and cleanliness
• Grooming – i.e. combing hair
• Eating
• Level of mobility
• Transferring
• Recreational activities
• Speech and higher functional abilities of the patient

Whether physiotheraphy & Occupational therapy started?

PMHx : Previous similar episodes
Drug Hx : Anticoagulants , Antiplatelets
Family Hx : DM , HT , Young onset stroke
Social history
• This is extremely important in this case. Take a detailed social history based on the points
given below
• Introduce the family – family members, income, social circumstances
• Describe the household environment in detail especially highlighting any barriers and
dangerous areas for the patient
• Assess the family support for the patient / Social support available
• Ask for the nearest hospital with rehabilitation facilities available

Examination
General examination

• GCS
• BMI
• Neck stiffness (sub arachnoid haemorrhage)
• Pallor/plethora (plethora could indicate polycythaemia which is a risk factor for stroke)
• Peripheral stigmata of hyperlipidaemia
• Look for features suggestive of vasculitis
• Look for peripheral stigmata of infective endocarditis
• Examine for bed sores
Neurological examination

• Examine all components of the nervous system and try to localize the lesion
Cardiovascular system

• Examine the pulse for arrhythmias ,BP , Apex

• Auscultate the heart for murmurs (MS)
• Examine the neck for carotid arterial bruits
Respiratory system

• Look for evidence of pneumonia

Abdomen
Summary
………………………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………………………
………………………………………………………………………………………………………………………………………………………
 Management

Initial management

1. A,B,C
2. GCS, vital parameters (pulse, blood pressure, respiratory rate, temperature)
3. neck stiffness
4. Investigations
FBC,ESR, CRP, serum creatinine, blood urea, serum electrolytes, plasma glucose, plasma
lipids, liver function test, ECG, echo, carotid duplex
5. Brain imaging -it's not possible on clinical grounds alone to reliably differentiate between
ischaemic stroke and intracranial hemorrhage

brain imaging- mandatory- should be done immediately at least within 24 hours to exclude
haemorrhagic stroke and other causes of focal neurological lesions
NCCT scan- normal in the ischaemic stroke when performed in the first few hours. 100%
sensitivity for hemorrhage

General treatment of acute stroke

Salvage ischaemic penumbra – Prevent hypotension , Hyperglycemia, pyrexia

 BP often elevated and falls spontaneously within first few days

 Mx– Continue existing anti-hypertensive

o Active treatment of blood pressure if >220/120 mmHg in cerebral infarction
o Hypoxia –ischaemic tissue susceptible to secondary hypoxia
 Oxygen should be given if hypoxia develops
o Hyperglycemia – Increased death

 Fever management
 Management of dehydration and swallowing
 Early mobilization

Specific treatment of acute ischaemia

Aspirin 300 mg and continue once diagnosis of ischaemic stroke has been made

Thrombolytic agents –rTPA

Indications
Age >18 years
Clinical Dx of ischaemic stroke causing a measurable neurological deficit
Onset within 4.5 hours

Contra indications

 Minor or rapidly resolving stroke symptoms

 Other stroke or serious head trauma within past 3 months
 Known Hx of ICH
 Sustain SBP >185 mmHg or DBP > 110 mmHg at the time treatment is to begin
 Symptoms suggestive of SAH
 GI or GU haemorrhage within past 21 days
 Arterial puncture at a non-compresssible site within past 7 days
 Patient received heparin within the last 48 hours and has elevated APTT
 Plt count <100000 per microliter

Malignant middle cerebral artery syndrome

Severe proximal middle cerebral artery or internal carotid artery infarction producing cerebral
oedema and increased intracranial pressure and brain herniation, causes hemiparesis,
hemianaesthesia, head turning and eye deviation.

Peak incidence at 3-5 days subside by 14 days

Increased incidence with CT > 50% of brain area involvement, midline shift of septum
pellucidum>5mm, infarction of additional vascular territories

Definitive treatment is decompressive hemi craniectomy

Treatment of acute intracerebral hemorrhage

Indication for surgical evaluation of hematoma

 cerebellar hemorrhage >3 cm in diameter in patients with deteriorating level of
consciousness, brainstem compression and/or hydrocephalus due to ventricular obstruction
 supratentorial lobar clots > 30 ml when 1 cm of the surface in patients with clinical
deterioration
Prolonged fever

Presenting complaint
• Fever for ………………. duration

History of the presenting complaint

Symptom analysis

1. Analysis of fever

• Describe the onset of the fever and state if there are any specific preceding events
• Describe the onset and progression of the fever
• Describe the fever pattern and based on the history- this is best done using a graphical
representation of the fever
• State the temperature at the height of the fever, the duration of a fever spike and the
duration of the fever free period
• Describe the symptoms associated with a fever spike – chills and rigors
• Also go on to state how the patient feel in between episodes of fever
• Response to paracetamol
• Next think of the possible differential diagnosis and ask specific questions

Fever Description Clinical Eg:-

pattern
Intermittent Pyogenic infections
TB
Lymphoma
systemic onset JIA

High
spiking fever which reach baseline
Remittent Viral infections -
CMV
IE
Lymphoma
Amoebiasis
Kawasaki

Fluctuating fever , does not reach baseline

 Continuous Typhus
Typhoid (slow
stepwise and high
plateau)
Lobar pneumonia
UTI
Little or Brucellosis
no fluctuation

Relapsing Malaria
Lymphoma

Febrile episodes separated by 1 days w/o fever

2.Aetiology

Aetiology Clinical features

Tuberculosis Prolonged fever
Nocturnal fever
Cough and haemoptysis
night sweats
LOA
LOW
Contact history
treatment at welisara
Lymphoma Neck lumps
(Haematological malignancies) features of anaemia and polycythaemia
bone pain
recurrent infections
Infective endocarditis Past history of cardiac disease
Rheumatic fever
Dental caries
predisposing invasive procedures (genitourinary procedures)
prophylaxis antibiotic taken correctly prevent IE.
IV drug use
Connective tissue disorders(esp Joint pain
SLE) rashes
oral ulcers
haematuria
proteinuria
Malaria Fever pattern
visit to endemic area
Typhoid History of unhygienic food consumption
high spiking fever
 alternating constipation and pea soup diarrhoea
rose spots in abdomen
Right iliac fossa pain
HIV Unsafe sexual practice
Iv drug abuse
blood transfusion
Solid organ malignancies
-Hepatoma RHC pain
jaundice

-Renal cell carcinoma Haematuria

loin pain
loin mass
UTI Frequency
Dysuria
Haematuria
IMN Sore throat
Chronic meningitis Headache
adult onset seizures
focal nuerological signs
Drug fever Especially antibiotic use

Complications
IE – Heart failure
- Arrythmias (palpitations)

Treatment upto now

Investigations done –Blood culture

Echo
CXR
Bone marrow
Mantoux
Social History- Ask about hobbies, pets, travel history
Examination
General examination

Perform a thorough general examination

Eyes

• Look for pallor and Icterus

• Red eye associated with connective tissue diseases
– uveitis and scleritis
 • Examine the fundus for Roth spots in infective endocarditis (see picture) and choroidal
tubercles in TB

Head and neck

• Examine for cervical lymphadenopathy

• Examine the ears for discharge and the tympanic
membrane

Mouth

• Look for dental caries

• Inflamed throat, tonsillar enlargement

Hands and fingers

• Finger clubbing
• Splinter hemorrhages
• Janeway lesions
• Vasculitic lesions

Skin

• Skin rashes
• IV injection sites
• Venous catheters

• Bone marrow site

CVS

Look for murmurs (IE)

RS

• Examine for features of consolidation or pleural effusion (TB)

Abdomen

• Look for hepatosplenomegaly

-CLD and portal hypertension
-EBV , typhoid , Haemolytic anaemia , Leukemia and lymphoma
-Glycogen storage disease

• Palpable masses in the abdomen

• Ascites
• Do not forget to examine the external genitalia
 • Do a per rectal examination

Musculoskeletal system

• Joint swelling and tenderness

Nervous system

• Signs of meningism (chronic meningitis)

• Focal neurological signs

Discussion
What is the definition of pyrexia of unknown origin?
• PUO is defined as fever > 38.3 degrees Celsius on several occasions
• Lasting for more than 3 weeks
• Where a cause has not been found after1 week of rational inpatient investigations or 3
outpatient visits

What is you diagnosis or differential diagnosis?

• diagnosis or differential diagnosis should be based on the history and examination

History Examination Differential diagnosis

PUO Peripheral stigmata of IE (rare) Infective endocarditis
Past history of rheumatic fever/ Cardiac murmur
congenital heart disease (MR, AR)
PUO Pleural effusion TB
Chronic cough, hemoptysis
+/- Contact history of TB
PUO Pallor Leukaemia Lymphoma
+/- symptoms of bone marrow Lymphadenopathy
suppression Hepatosplenomegaly

The initial investigations

This will be based on clinical diagnosis or differential diagnosis
Clinical diagnosis Investigations What to look for
IE Blood culture Echo These are required for the
confirmation of the diagnosis
TB CXR
Mantoux test
Hematological malignancy FBC Look for pancytopenia
Blood picture Look for abnormal cells (blasts)
USS of the abdomen Confirm the organomegaly
Look for para aortic lymph nodes
Bone marrow biopsy

Infective endocarditis

.
What are the principles of management of a patient with infective
endocarditis?
• A patient with infective endocarditis is usually managed medically. However there are
certain indications for surgical management
• The patient should be started on high dose intravenous empirical antibiotic therapy. This is
usually a combination of benzyl penicillin (1.2g IV for 4 days) and gentamicin (80mg bd for 2
weeks)
• Treatment is continued for a minimum of 2 weeks
• Surgery is indicated in the following circumstances
Severe heart failure due to valvular damage
Failure of antibiotic therapy
Large vegetations with evidence of systemic emboli
Abscess formation in the heart

Look for complications of the disease – Heart failure, evidence of systemic embolization
What are the causes for continued fever in a patient with infective
endocarditis?
• Incorrect antibiotic
• Inadequate dose
• Complications – abscess formation
• Distal embolization

Lymphomas

Hodgkin’s lymphoma Non Hodgkin’s lymphoma

Clinical Lymphadenopathy usually begins Has a more unpredictable and
from 1 group of peripheral lymph haphazard spread
nodes and spreads
contiguously to the others

Can have mediastinal involvement Involves oropharyngeal lymph

Extra nodal spread rare
Leukaemic phase rare
Constitutional symptoms
common
nodes
Extra nodal spread common
Leukaemic phase more common
Constitutional symptoms rare

Investigations Lymph node biopsy shows Reed – No RS cells

Sternberg cells
Management Early stage disease Multi agent chemotherapy
Radiotherapy

Advanced disease
Chemotherapy +/- radiotherapy
Chronic cough and hemoptysis

History
Presenting complaint
Haemoptysis for ………………..duration

History of the presenting complaint

Symptom analysis
• Describe the onset, duration and progression of the symptom
o Haemoptysis with purulent sputum for several years with LRTI – Bronchiectasis
o For few weeks could be lung carcinoma or Tuberculosis
o Pneumonia – Rusty sputum

• Describe the amount and nature of the sputum

o Mixed with copious purulent sputum – Bronchiectasis
o Massive haemoptysis – Tuberculosis , Bronchiectasis
o Foul smelling – Bronchiectasis , Lung abscess

• Think of a differential diagnosis and ask specific questions

Disease Specific points in the history

Pulmonary TB long standing fever, night sweats, anorexia and
malaise , Loss of weight
Past history or contact history of TB , Past history of
Treatment at Wellisara

Features of disseminated TB – Bone , Bowel and

brain
Bronchial carcinoma 1.Smoking
2.associated loss of appetite and loss of weight
3.Ask for recurrent LRTI
Progressive shortness of breath
Past history of malignancy (i.e. breast)-
secondary deposits
4.Features of local spread
Hoarseness of the voice (Recurrent laryngeal nerve)
Drooping of the eyelid (Horner’s syndrome)
Puffiness of the face and prominent veins in the
neck (SVC obstruction)
Small muscle wasting of hand – Pancoast tumour

Distant spread
LN
Neck lumps noticed by the patient
Liver
Right hypochondriacal pain and yellowish
discolouration of the eyes
Bone
Bone pain, history of fractures following trivial
trauma, difficulty in walking
Brain
Early morning headache with associated vomiting,
adult onset seizures

Paraneoplastic syndromes
Neurological
Seizures
Imbalance when walking (cerebellar degeneration)
Progressive difficulty in climbing steps (proximal
myopathy)
Weakness and numbness of the limbs (peripheral
neuropathy)

Endocrine
- Confusion and constipation (hypercalcaemia)
-Cushings symptom
- Drowsiness and confusion (SIADH)

Bronchiectasis Characterized by copious sputum production

sputum production change with position
Halitosis
Recurrent febrile episodes
Lung abscess Foul smelling sputum
Swinging fever
Vasculitis Ask for features of multisystem involvement,
Wegener’s granulomatosis especially joint manifestations and hematuria
Goodpasture syndrome suggestive of glomerulonephritis
Coagulopathy Other bleeding manifestations

Past medical history

Past surgical history
-Past hx of pneumonia , measles , Pertussis , TB

-Childhood recurrent chest infection

-Immuno compromised state

-Drug used (Anticoagulant)

Social history
• Get a detailed history of smoking
• Occupational history may also be extremely important
o Asbestos
o Chromium
o Petroleum
• Discuss how the disease affects the patients day to day life

Examination
General examination

• Look for cachexia

• Pallor and Icterus in the eyes
• Horner’s syndrome
• SVC syndrome
• Examine for cervical lymphadenopathy
• Examine the hands for clubbing and hypertrophic pulmonary osteo arthropathy (Bronchial
carcinoma)
• Look for wasting of the small muscles of the hand(Pancoast’s tumor)
Look for ankle oedema

Respiratory system

• Examine for evidence of a pleural effusion (malignancy, TB)

• Localized consolidation
• Bilateral basal crepts
• Lung collapse
CVS
Dextro cardia

Abdomen

• Hepatomegaly
• Ascites
Neurological

• Look for evidence of a paraneoplastic neurological syndrome

o Cerebeller symptoms
o Lower limb sensory and power
o Peripheral neuropathy
• LL weakness – bone metastasis

Discussion
Bronchiectasis

Investigations

 Chest x-ray – may be normal, ring shadows, rail road -usually in lung bases

 High resolution CT (HRCT)-most sensitive

 Other investigations
o Full blood count
o Sputum microbiological examination
o Lung function (spirometry)

 In selected cases
o X-ray sinuses
o Serum immunoglobulin levels
o CF genetic studies
o Alpha-1 antitrypsin levels
o Skin testing for aspergillus

Treatment

 Bronchial hygiene
o Hydration
o Nebulized saline
o Postural drainage
o Active cycle breathing technique
o Mechanical devices for sputum clearance

 Mucolytic agents (nebulized acetylcystein)

 Avoiding infection
 Antibiotics (long term cyclical antibiotics or intermittent antibiotics for recurrent or persistent
infection)

 Bronchodilators (for coexisting airway hyperactivity)

 Surgical
o Resection of a segment for localized bronchiectasis
o Bronchial artery embolization for massive bronchiectasis
o Lung transplantation

Acute infective exacerbation

 Increased sputum volume and viscosity

 Fever may be absent
 Organisms – H.influenzae, P.aeruginosa, S.pneumoniae
 Antibiotics-fluoroquinolone(ciprofloxacin)

Complications

 Haemoptysis (due to erosion of a nearby blood vessel)

 Lund abscess
 Empyema
 Lung fibrosis, cor-pulmonale, respiratory failure
 Pericarditis
 Sepsis, metastatic abscesses (brain)
Amyloidosis

Tuberculosis
Investigations
Mantoux test

• 0.1ml(10 units) of a PPD solution is injected intradermally into the flexor aspect of the
forearm
• Induration is read after 48-72 hours
• Induration > 10mm is considered positive
• However this test can be negative in patients with TB who also have HIV infection due to
impaired cell mediated immunity

Imaging investigations

• CXR is a first line investigation- Look for upper lobe fibrosis and cavities
• CT scan may be required in some cases
Microbiological investigations

• Sputum
Early morning expectorated samples of sputum on 3 consecutive days for acid fast bacilli
stain and culture in the Lowenstein- Jensen medium (done at welisara)

Special investigations

• Bronchial washings are used as microbiological samples in patients who cannot expectorate
sputum
• Pleural effusion aspirate – AFB and adenosine deaminase levels
Pleural biopsy in selected patients

How would you manage this patient?

• Isolate the patient
• Educate the patient on the disease, proper disposal of sputum
• Educate the patient on the importance of compliance to drug therapy and on the side effects
of the medication
• Do the baseline investigations prior to the commencement of therapy. Liver function tests
are the most important
• Start the medical management
Intensive phase – Isoniazid, Rifampicin, Pyrizinamide and Ethambutol daily for 2 months
Continuation phase – Isoniazid and rifampicin for 4 months

Drug and mechanism of action Dose Side effects

Isoniazid 5mg/kg Liver toxicity
Bactericidal and bacteriostatic Peripheral neuropathy
effect Mental disturbances
Incoordination
Drug interaction – enzyme
inhibitor
Rifampicin 10mg/kg Liver toxicity
Bactericidal effect Orange discolouration of body
secretions
Skin rashes, thrombocytopenia
Oral contraceptive failure
Pyrizinamide 25mg/kg Liver toxicity
Kills intracellular persisters Hyperuricaemia
Ethambutol 15mg/kg Optic neuritis
Bacteriostatic effect
How would you follow up this patient following the initial treatment?
• Regular follow up during the 1st 2 months. In ward treatment at Welisara chest hospital is an
option
• DOTS may be employed in the community
• See the patient after 2 months Assess the symptoms
Examine the patient
Assess the adverse effects of drug therapy
Repeat the chest x ray
Sputum samples
Liver function tests
• If the sputum smear is positive at 2 months repeat another smear at 3 months. If this is
positive perform drug susceptibility testing

What are the other aspects of management in a patient with tuberculosis?

Contact tracing and prophylaxis

• Perform mantoux test and CXR in close contacts

Indications for treatment - Isoniazid is the Drug of choice

• Adults with symptoms of TB

• Adults with CXR changes suggestive of TB
• Children with a positive mantoux test

How would you treat multi drug resistant TB?

• Complex treatment regimens

• Second line anti TB drugs

Quinolone-oflxacin,ciprofloxacin
Aminoglycoside- Kanamycin, Amikacin, Capreomycin
Para amino salicylic acid-cicloserine, Ethiopromide
Macrolide- Clarithromycin, Azithromycin
Bronchial carcinoma

Investigations
 CXR
 CT
 Fiberoptic bronchoscopy
 Percutaneous aspiration and biopsy

Treatment
 Surgery – can be curative in non-small cell lung cancer
 Radiation therapy for cure (Radiation pneumonitis)
 Chemotherapy
 Laser therapy, endobronchial irradiation, Stents
 Palliative treatment