Short Cases

Physical Diagnosis Guide for Internal Medicine Exams

Physical diagnosis exams, commonly known as short cases, are part of the assessment
carried out by the departments of Internal Medicine and Pediatrics to evaluate the
readiness of medical students to function as physicians. Medical students will face these
exams starting from their clinical year I attachment all the way to the qualification exam.
These moments have proven to be very stressful and unpleasant. But, that probably
wouldn’t be the case with focused preparation.

Short case exams usually involve not only physical examination, but also:

A complete report of the findings, both positive and unremarkable

Interpretation of the findings
Differential diagnosis and
Possible investigation modalities

The examiners mainly grade the student based on the performance s/he displayed on the
above parts of the exam. However, other activities may raise the status of the student in
the eyes of his/her grader, including the use of alcohol (hand rub) to disinfect the hands,
introducing oneself to the patient and asking consent, maintaining eye contact to check for
tenderness and showing an attitude of respect for patients as well as examiners.

Good luck!
 Examination of the Chest
The respiratory system consists of organs that are involved in conveying air
from the outside environment to the place of exchange of gases with the
blood…
01

Precordial Examination
The cardiovascular system as the name indicates, consists of the heart and
the vessels that distribute the blood that is ejected from the heart.
Examination of the…
08

Examination of the Abdomen

The abdomen houses some of the most important structures in the human
body including the liver and the kidney. Other important structures such
as the stomach…
12

Lower Motor Examination

Normal motor function is a result of integrated activity between the
cerebral cortex, internal capsule, basal ganglia, cerebellum, spinal cord,
peripheral nerves & muscles. Any abnormality...
20

Examination of the Lymphatic System

The lymphatic or lymphoid system comprises the lymph, the lymphatic
vessels, lymph nodes, the thymus and the spleen. But, for short case
exams, this section will give emphasis…

26
 Examination of the Chest
Compiled by: Michael Yeshiwas

The respiratory system consists of organs that are involved in conveying air from the outside environment to the place
of exchange of gases with the blood. By this logic, it includes all of the airway and the lung. However, one should not
forget the implication of respiratory muscles such as the diaphragm in the process of respiration.

Patients with diseases of the lung or the airway may display signs elsewhere, including clubbing of the fingers,
central/peripheral cyanosis, flaring of ala nasi, use of accessory muscles of respiration and others as well. There may
also be deformities of the chest wall, some seen on the anterior and others on the posterior chest. Counting the rate
and characterizing the pattern of respiration is also important. As a result, a respiratory system examination is said to
be complete only if it considers manifestations of respiratory diseases around the chest as well as other areas of the
body. Nonetheless, the respiratory examination of the exams largely focuses on the posterior chest. Thus, it is important
to know the difference between respiratory examination and examination of the posterior chest, as the latter is a
component of the former.

Examination of the Chest In appearance we should look for:

Like other examinations, this also depend on the four
steps, i.e. inspection, palpation, percussion and finally
auscultation. Unlike the anterior chest examination
which is done in semi-recumbent position with
abducted arm, the posterior chest is better examined
with the patient sitting upright with arms folded across
the chest.
Scar: which can be surgical or traumatic
Dressing: after drainage of pleural fluid (may
even give you an idea on where to expect a
pleural effusion)
Prominent veins: mostly on the anterior chest
due to superior vena caval obstruction
Symmetry of the chest comparing the right and
the left sides
Shape of the chest: different deformities in the
anterior and posterior chest

Barrel chest: is when AP diameter of the chest is

If the patient is not acutely ill, it is better if s/he sits on
the edge of the bed, undressed up to the waist.
Inspection
increased compared to the lateral, indicating
hyperinflation (severe asthma or emphysema)
In the anterior chest:
Pigeon chest: alternatively known as pectus
carinatum, represents localized outward bowing of
the sternum and costal cartilage. It is a sign of either
rickets or chronic childhood respiratory illnesses.
Funnel chest: also known as pectus excavatum, it is
the reverse of the previous. It involves a localized
depression in the lower sternum and may restrict
lung capacity in severe cases. It is a result of a
developmental defect.

In the examination of the chest, inspection can be
summarized as ‘ABC’, where A stands for appearance, B
for breathing and C for chest movement. It is important
to report even what might be considered trivial.
Harrison sulcus: like a pigeon chest, this is due to
rickets or childhood asthma. You can see it as a linear
depression of the lower rib above the costal margins
at the site of attachment of the diaphragm.

01
 In the posterior chest:
Kyphosis: is an exaggerated forward curvature of the
spine (thoracic spine)
Scoliosis: is lateral bowing of the spine
Kyphoscoliosis: is a combination of the above two,
which can be idiopathic or secondary to poliomyelitis
or marfan syndrome. If severe enough, it can lead to
reduced lung capacity and increased work of
breathing.
The chest movement should also be assessed by placing
your hands firmly on the chest wall with the fingers
extending to the side of the chest and the thumbs
placed to the midline, to the point that they almost
meet. To see the chest movement, the thumbs should
be slightly lifted off the chest wall. Then ask the patient
to take deep breath in. In a normal condition the
thumbs should be moved apart symmetrically during
inspiration. If the movement is reduced in one side, you
should suspect a problem on that same side.

Despite its overlap with the precordial examination, you

should also see if there is a precordial bulge in anterior
chest examination, as it indicates a long standing
cardiac condition, which may have respiratory findings.

In breathing we can see the breathing pattern, count

the respiratory rate (14-20 beats/min in adults) and
assess the depth of respiration.

In chest movement, you should see the symmetry and

reduction in the chest movement:

Unilaterally diminished movement indicates

conditions such as consolidation, fibrosis,
collapse, pleural effusion or pneumothorax in Differentials for reduced chest movement
the same side of the decreased movement. Pleural effusion
Bilateral reduction of chest wall movement pneumothorax
points to diffuse abnormalities like COPD and Consolidation
diffuse pulmonary fibrosis. Collapse
Palpation Fibrosis

If you are asked to do an anterior chest examination, the Chest expansion measurement is the other examination
first step in palpation should focus on the trachea. You during palpation. It involves measuring the difference
can place the pointer and ring fingers on the sides of the between the chest circumferences during inspiration
suprasternal notch and use the middle finger for and expiration just below the nipples, using a tape
palpation. Even in a healthy person, the trachea may be meter. Normally, the circumference is higher during
slightly deviated to the right. But a significant deviation inspiration by more than 5cm and a difference that is
to either side should be considered abnormal. less than 2cm is definitely abnormal.
Displacement to the side of the lesion is due to
upper lobe collapse or fibrosis.
Displacement to the opposite direction can be
caused by any condition that push the trachea
away: massive pleural effusion or tension
pneumothorax. Other than these differentials
you can also consider any intra-thoracic mass
(lymphomas, cysts, retrosternal thyroid and
others).

You should also palpate the chest wall to see if there is

tenderness, suggesting rib fracture or other traumas.

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A small expansion suggests generalized conditions Due to hyper-inflation like:
limiting expansion of the lungs (bronchial asthma, Hyper-resonant Emphysema
emphysema and pulmonary fibrosis) or those limiting Asthma
the movement of the ribs (ankylosing spondylitis). Pneumothorax
Due to fluid in the thorax like:
Tactile vocal fremitus is the last step in palpation. In this
Stony dull Pleural effusion
examination, you just try to appreciate the sound
Hemothorax
transmitted to the chest wall as low frequency
Empyema
vibration. Certain words are known to better create
Due to conditions like:
such effect (ninety nine or ‘Arba Arat’ in Amharic
Dull Consolidation
speakers). You should compare both sides of the chest
Lung fibrosis
and decide whether it is increased, decreased or as it is
Lung collapse
the case most of the time, normal.
Pleural thickening
An exaggerated tactile fremitus is due to
Although not done frequently in the current time,
consolidation and a depressed fremitus can be due
diaphragmatic excursion is also another examination to
to pleural effusion, pneumothorax or pleural
be done in percussion. First, percuss along the scapular
thickening.
line on one side until the level of the diaphragmatic
In some literatures, you may find a crepitation, listed on dullness. Then ask the patient to inspire deeply and hold
palpation. This is not the same as the crepitation heard his/her breath in. Proceed to percuss down from the
by auscultation, but heard without the aid of a marked point to determine the diaphragmatic excursion
stethoscope, when palpating on the surface of the in deep inspiration. Measure the distance between the
chest, if there is a subcutaneous emphysema. upper & lower points in cm. This should be done on both
the right and left sides. Excursion is normally 3-5cm and
Percussion
symmetrical on both sides.
Percussion should be done by hyperextending the
Auscultation
middle finger of one hand and placing the distal inter-
phalangeal joint firmly against the patient’s chest. Then The purpose of auscultation is to detect the air entry,
strike it with the end (not pad) of the opposite middle listen to breath sounds and added (adventitious)
finger, with a quick flick of the wrist. sounds.

Percuss symmetrical (equivalent) areas of both sides
(including apices, posterior, lateral, & anterior) of the
chest at about 5cm intervals from the upper to the
lower chest (moving from left to right & right to left) and
compare both areas.
Just like palpation and percussion, auscultation should
be done in an organized way, i.e. once you listen on a
certain area in one side of the chest, you should listen
to the corresponding area on the other side before
going inferiorly. This will allow better comparison.

The air entry should be characterized as normal,

increased or decreased to the level of absence. Lung
consolidation and fibrosis are known to increase the air
entry as characterized by the intensity of the sound.

Decreased/absent air entry Increased air entry

Pleural effusion Consolidation
Pneumothorax Fibrosis
Hemothorax
Lung collapse
Severe asthma
Emphysema
Major bronchial
The normal percussion note in the chest is resonant.
obstruction
Any other note is considered as an abnormal finding and
include hyper-resonance, dull and stony dull (flat).

03
In general, anything that increases the space between The last auscutatory finding may be added sounds.
the lung and the chest wall decreases sound intensity Alternatively, they can be called adventitious sounds
(pneumothorax, pleural effusion and hemothorax). and include:

You should also listen to breath sounds like: Crackle: also known as crepitation or rale is a
short crackling sound heard during inspiration,
Vesicular: longer inspiration phase compared to
when collapsed alveoli are expanded.
the expiration and no pause between the two. It
Rhonchi: continuous sounds produced when
is the sound of a normal lung parenchyma.
there is a free fluid in the airway lumen.
Broncho-vesicular: it is normally heard at the
Wheeze: a predominantly expiratory musical
areas of the major bronchi, especially at the
sound, heard when there is airflow limitation.
sternal border and apex of the right lung.
Pleural friction rub: creaking noise that is similar
Bronchial: equal inspiratory and expiratory
to the noise created by compression of a new
phases and there is a gap between the two. It is
leather, indicating an inflamed pleural surfaces
normal only when heard on the trachea.
rubbing against each other. Usually heard both
Amphoric: It is a sound heard like that made by
during inspiration and expiration.
blowing over the mouth of a narrow necked
Stridor: similar to wheeze, but predominantly or
bottle.
entirely inspiratory. It is due to a narrowed
Normal Pathologic airway outside the thorax (mostly the trachea).
The trachea Consolidation
Differentials
Bronchial Fibrosis
Fine crepitation
Lung collapse
Crackle Pulmonary edema
Over the top
Fibrosing alveolitis
of pleural
Coarse crepitation
effusion
Bronchiectasis
None Cavitary
Bronchogenic pneumonia
Amphoric lesions
Rhonchi Free fluid in the airway
Over the top
Bronchial asthma
of pleural
Wheeze Bronchitis
effusion
Laryngeal spasm
Vocal resonance is an important examination, especially
Tracheal fibrosis
if consolidation is suspected. Normally, the patient’s
Congestive heart failure
speech is heard through the chest wall as a muffled
Intraluminal obstruction by
voice. But, in consolidation of the lungs the following
tumors or secretions
may be heard:
Friction rub Inflammation of the pleura
Broncho-phony: ask the patient to say ninety Tuberculosis
nine/arba arat repeatedly and auscultate Pneumonia
several symmetrical areas over each lung. Pulmonary infarction
Normally, you should hear muffled and Stridor Croup
indistinct sounds. If a loud and clear sound is Epiglottitis
heard, we call it broncho-phony. Foreign body
Whispered Pectoriloquy: ask the patient to Mass lesion
whisper ninety nine/arba arat and auscultate. Anatomical defect
Normally, you hear a faint sound or nothing at External obstruction
all. Whispered pectoriloquy is when you hear How do you differentiate pleural friction rub with
the sound clearly. pericardial friction rub? If the origin is pleural, the sound
Egophony: ask the patient to repeatedly say ‘E’ will disappear when breathing is stopped, as there will
and auscultate. Normally, you hear a muffled E, be no friction between the inflamed pleura. But, if it is
but if you hear an ‘A’, we call it an egophony. of pericardial origin, you will still hear the sound as the
heart will continue beating anyway.

04
 Disorder Findings
Reduced chest wall movement
Consolidation Dull on percussion
(top differentials are Bronchial breath sound
tuberculosis and pneumonia) Crackles
Mediastinal shift to the affected side
Collapse Reduced chest wall movement on the affected site
Dull on percussion
Absent/reduced breath sound
If massive, mediastinal shift away from the affected side
Reduced chest wall movement on the affected side
Pleural effusion Stony dull on percussion
(many differentials based on Absent breath sound over the fluid, may have bronchial breath sound above
the pleural fluid analysis) the effusion
May have friction rub above the effusion
If under tension, mediastinal shift away from the affected side
Pneumothorax Reduced chest wall movement on the affected side
Hyper-resonant on percussion
Absent or greatly reduced breath sound
Reduced chest wall movement symmetrically
Bronchial asthma Normal or reduced breath sound
Wheeze
Interstitial pulmonary fibrosis Reduced chest wall movement symmetrically
Fine late or pan-inspiratory crackles over affected lobes

Common Investigations Reading the x-ray in a sequential manner is preferable:

1. Sputum Examination Trachea: central or deviated

Mediastinum: widening or shifting
Sputum examination starts with its appearance. A Hilar shadow: size/shape, lymphadenopathy
yellowish-green sputum is generally suggestive of an and pulmonary artery shadow
inflammation (allergic or infectious). If the sputum is
Diaphragm: elevated or flat, gas under the
blood tinged, you can suspect acute infections, TB, diaphragm, obliteration of the costophrenic
tumor or pulmonary infarct.
angle (pleural effusion)
Gram stain may prove to be useful in lower respiratory Lung fields: apical haziness is suggestive of
tract infections or aspergillus lung disease. tuberculosis. You should look for infiltrates
(homogenious/patchy), reiculo-nodular pattern
Sputum AFB has low specificity and sensitivity, so it is
(TB), fibrosis, opacities, cavities and prominent
largely replaced by gene X-pert. Gene X-pert also have
vascular markings.
the added benefit of identifying drug resistance,
Pleural space: wide pleural space with no lung
particularly to rifampicin.
marking is suggestive of pneumothorax. You
Sputum cytology can be important in the diagnosis of can also see pleural thickening.
bronchogenic carcinoma. If the patient is not producing
In a complete chest x-ray reading, the patient’s personal
sputum, you can induce it by nebulized hypertonic
information (name, age and sex) should be included and
saline or obtain it during bronchoscopy in bronchial
a comment on the soft tissue and the bony tissue is also
washing.
a component.
2. Chest X-ray
3. Chest CT scan
It should be taken in full inspiration so that the lower
It can assess the size and position of pulmonary masses
parts of the lung are seen clearly.
and nodules.

05
CT can also show cavitary lesions and calcification. Its
role in the staging of bronchial carcinoma is also
undeniable.
High resolution CT scanning samples the lung
parenchyma in a 1-2mm thickness, making it effective in
the diagnosis of interstitial lung disease, bronchiectais
and emphysema.
4. Ultrasound
Ultrasound is particularly useful for the detection of
pleural effusion, especially if loculated.
5. Ventilation-perfusion scan
It is important in the diagnosis of pulmonary embolism,
where we expect to see a diminished perfusion relative
to ventilation.
6. Bronchoscopy
Although not useful in every situation, there are
occasions where the role of bronchoscopy can be
irreplaceable. It have the dual advantages of looking
directly at the lesion and taking specimen for cytology,
histo-pathology and bacteriology.
7. Pulmonary function tests
It is an important investigation modality if you suspect
a condition that may impair the ability of the respiratory
system to perform its main function of gas exchange:
particularly asthma and COPDs.
The pleural fluid can be classified as exudative and
transudative based on the light’ criteria.
Lights’ criteria
Exudative fluid is when
Pleural fluid protein to serum protein ratio of
> 0.5
Pleural fluid LDH to serum LDH ratio of > 0.6
Pleural fluid LDH > 2/3rd of the highest normal
serum LDH value for the laboratory
The reverse would be transudative.
Modified Lights’ criteria is a newer version where the
cutoff for the protein is 0.45 and LDH is 0.5. It also
adds pleural fluid cholesterol (>45 is exudative).
Transudative pleural fluid is seen in:
Congestive heart failure
Nephrotic syndrome
Liver cirrhosis
Exudative pleural fluid is seen in:
Malignancies
Tuberculosis
Pneumonia
Empyema

8. Pleural biopsy

It is a procedure associated with many complications

and should adhere to the indications. It is the gold
standard for the diagnosis of tuberculosis.

9. Pleural fluid analysis

Pleural fluid analysis is a simple procedure which is very

important for the exam. This investigation lifts more
than its weight, as there is no examiner who wouldn’t
want to hear in detail about it.

Analysis of the pleural fluid starts from the appearance

or color. A straw colored fluid (color of a concentrated
urine) suggests tuberculosis. A bloody fluid is suggestive
of either malignancy or infection. A whitish fluid is a
chyle, suggesting lymphatic origin. An empyema yields
a literal pus as a fluid.

The pleural fluid can be sent for many investigations

such as gene X-pert, AFB and culture. But another very
important investigation to narrow differentials is
biochemical analysis including protein and LDH.

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Summary of Chest Examination

1. Inspection
Scar
Dressing
Prominent veins
Symmetry of the chest, chest expansion
Shape of the chest (deformities in the anterior and posterior chest)

2. Palpation
Tenderness
Tracheal deviation
Chest movement
Chest expansion
Tactile fremitus

3. Percussion
Percussion note
Diaphragmatic excursion

4. Auscultation
Air entry
Breath sounds
Vocal resonance
Added sounds

07
 Examination of the Precordium
Compiled by: Minale Menberu

The cardiovascular system as the name indicates, consists of the heart and the vessels that distribute the blood that is
ejected from the heart. Examination of the cardiovascular system is thus not only about the precordium but also
consists of:

General examination: for peripheral and central cyanosis, clubbing of fingers, oslers nodes, janeway lesions,
splinter hemorrhage, pallor for anemia and others.
Arterial examination: blood pressure and pulse (rate, rhythm, volume, character and condition of vessel
wall) should be assessed. The pulse of the carotid, brachial, radial, femoral, popliteal, dorsalis pedis and
posterior tibial arteries should be assessed. You should also check for radio-radial and radio-femoral delay.
Venous examination: involves JVP (jugular venous pressure) measurement from the angle of Louis and
checking for hepato-jugular reflux. You should also look for abnormal venous distention over the neck and
thoracic wall, varices, phlebitis and pedal edema.

The precordial examination follows all these steps. But, in exams you are more likely to be ordered to do the precordial
examination, instead of the cardiovascular examination. As a result, it have been discussed in detail.

Precordial examination Precordial movement (activity): we say that the

Similar to other examinations, there are tasks that
should be carried out before starting your examination
and these include:
Introduce your self
Maintain adequate illumination
Avoid noises and respect privacy (not applicable
in the Tikur Anbessa examinations)
Stand on the right side of the patient unless you
are left handed
Follow antiseptic technique
Position the patient appropriately
Warm your stethoscope and hands by rubbing,
never by blowing air out of your mouth
After the above parameters are secured, you can start
the precordial examination.
The first step is inspection and you look for:
precordium is active when there is pulsation in more
than one site.
An active precordium can be seen in regurgitant
lesions, congenital heart diseases (ASD, VSD,
and TOF) and high output states (thyrotoxicosis,
pagets disease, anemia and arterio-venous
fistula).
Quite precordium can be seen in a normal heart,
restrictive cardiomyopathies, constrictive
pericarditis, mitral stenosis and morbid obesity.
Apical impulse: it is the most lateral and downward
positioned impulse and usually lies in the 5th intercostal
space medial to (or on) the left midclavicular line. You
can report it as lateral or medial to the left midclavicular
line by centimeters. When you do this, it is important to
measure the clavicle and assume a midline, and draw an
imaginary line downwards.

Scar (especially surgical) The next step is palpation and you check for:

Visible vasculature in the area Palpable hear sounds: on the second intercostal spaces,
on both the right and left sides. If you palpate a heart
Precordial bulge: it shows long standing cardiac diseases
sound on the right (aortic valve area) you should
such as congenital heart disease or rheumatic heart
suspect systemic hypertension, and if the palpable
disease. On your physical examination, it has the
heart sound is on the left (pulmonary area) pulmonary
implication of explaining some of your findings. For
hypertension. There may be a palpable heart sound on
instance, a mitral stenosis can be explained by a long
the mitral and tricuspid areas in a normal person, so
standing rheumatic heart disease.

08
palpating those areas is pointless. It is better to palpate
with you index and middle fingers.
Point of maximal impulse (PMI) is usually located at the
same area to the apical impulse. Normal location is at
the 4th or 5th intercostal space just medial to the
midclavicular line. Characterizes the PMI in the
following manner:
Location: in relation with intercostal space and MCL
Size: in relation to area and number of inter space
Duration: in relation to systolic timing
Amplitude: feel the power (thrusting if forceful,
taping if not)
If the PMI involves more than one intercostal space or if
it spans for > 2.5cm (2cm in some literatures) we call it
a diffuse PMI and shows enlarged left ventricle
(hypertrophy or dilatation). If not, we call it a localized
PMI and rules out left ventricular enlargement.
In relation to systolic timing, if the PMI stays for > 2/3rd
of the systolic time we say that it is sustained and
indicates left ventricular enlargement. If < 2/3rd it is
tapping.
Thrills (a palpable murmur): should be checked at each
valvular site and we should palpate the site with bulb of
distal palm and spread our finger in interspaces. Then
compare it with a peripheral pulse like the carotid (if it
is synchronized with the pulse it is a systolic murmur,
and if not, a diastolic).
Heaves can be checked by placing your hands on the
three areas: apex, left parasternal and right parasternal
areas.
Apical heave: left ventricular hypertrophy
Left parasternal heave: right ventricular or left
atrial hypertrophy
Right parasternal heave: right atrial hypertrophy
You can differentiate if the left parasternal heave is
from the right ventricle or the left atrium. If the heave
synchronizes with the PMI, then it is of a ventricular
origin and if not atrial.
Percussion is not routinely done in precordial
examination and done for few indications:
Dextrocardia
Significant mediastinal shift
Cardiac delineation
Auscultation is performed symmetrically over 5
locations on the anterior chest wall. Use the diaphragm
of the stethoscope and switch to the bell to hear to low
pitched sounds (A M or M A).
A: Aortic valve, 2nd ICS on the right sternal border
P: Pulmonic valve, 2nd ICS on the left sternal border
E: Erb’s point, 3rd ICS on the left sternal border
T: Tricuspid valve, 4th ICS on the left sternal border
M: Mitral valve, 5th ICS left midclavicular line
The diaphragm better picks high pitched sounds: S1, S2,
pansystolic murmurs.
The bell better picks low pitched sounds: S3, S4,
diastolic murmur at apex.
You can use many maneuvers to enhance your findings.
Roll the patient to left side (left decubitus) and
auscultate apex: accentuate S3 and mitral
murmurs
Sit up and lean forward: accentuate diastolic
murmur of AR and pericardial friction rub
Hold breathing on:
Inspiration exaggerate right sided murmur
Expiration exaggerate left sided murmur
Valsalva decreases all murmurs except systolic
murmur of HOCM (hypertrophic obstructive
cardiomyopathy) and late systolic murmur of
MVP (mitral valve prolapse).
Any maneuver that increase LV after load (like
hand grip and vasopressor) will intensify
murmurs of MR, AR, and VSD.
In auscultation you need to listen to both the normal S1
and S2 sounds and other added sounds. You report it as
S1 and S2 are well heard or muffled…
Gallop rhythm (S3 and S4)
S3 shows rapid ventricular filling and seen in:
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 Left/right ventricular heart failure
Mitral regurgitation
Constrictive pericarditis
Anemia
Pregnancy
Fever
Thyrotoxicosis
S4 shows atrial contraction against non-compliant
ventricle and is almost always pathological. It is seen in:
Hypertension
Aortic stenosis
Hypertrophic cardiomyopathies
Opening snap can be heard in MS and TS
Pericardial friction rub (nearly 100% specific for
diagnosis of acute pericarditis): it is a rubbing sound
that is heard during systole and diastole, not affected by
holding breathing.
Pericardial knock is heard in constrictive pericarditis
Murmurs; abnormal sound due to turbulence of blood
flow. They can be either innocent (physiologic) or
pathologic.
Innocent: anemia, pregnancy, thyrotoxicosis,
fever...
Pathologic: valvular lesions, structural heart
disease
Characterization of murmur;
Timing: systolic, diastolic or continuous
Location of maximal intensity determines where
murmurs originate. Generally, murmurs are best
heard on site of their valvular area, except AR
which is best heard at Erb’s point.
Quality: harsh, blowing, rumbling, musical
Generally, early systolic murmur (AS/PS) is
harshs, early diastolic murmur (AR/PR) is
blowing and mid diastolic murmur (MS/TS) is
rumbling.
Radiation: reflect the intensity and direction of
blood flow
Pitch: high, medium or low
Intensity: is graded as:
G1: faint
G2: quiet but heard immediately
G3: moderately loud
G4: loud + thrill
G5: heard in a partially off stethoscope + thrill
G6: heard in full off+ thrill
Report like this: there is a grade 4, high pitched,
blowing, early diastolic murmur, best heard at right 2nd
ICS (aortic area) and without a radiation.
Types of murmurs with differentials are stated below.
Systolic ejection murmur (high pitched and harsh) can
be an innocent murmur (pregnancy, anemia, fever,
childhood…) or based on the site of the murmur, it can
be secondary to pathologic conditions such as:
Aortic stenosis and aortic sclerosis
Hypertrophic obstructive cardiomyopathy
Pulmonary stenosis
Atrial septal defect
Pansystolic murmur based on the site can be secondary
to MR, TR or VSD.
Diastolic murmurs are almost always pathologic.
Early diastolic murmur is high pitched and blowing.
Based on the site it can be due to AR or PR.
Late diastolic murmur is low pitched and rumbling. It
often starts after an opening snap. Based on the site
possible differentials can be:
Mitral stenosis
Tricuspid stenosis
Carey coomb’s murmur (due to thickened
mitral valve leaflet due to rheumatic valvular
heart disease, not preceded by opening snap)
Austin flint murmur (murmur of AR which can
be confused with mitral stenosis)
Large ASD
How to differentiate MS from Austin flint murmur?
Mitral stenosis murmur Austin flint murmur
Caused by rheumatic Caused by severe AR
heart disease
Follow an opening snap Follow an S3 gallop
Can have thrill Thrill is very rare
Signs of pulmonary Pulmonary hypertension
hypertension can be seen is unlikely
Continuous machinery murmur covering both systolic
and diastolic time can be secondary to:
PDA (best heard at pulmonic area)
Coronary AV fistula
Cervical venous hum
ASD + MS
Ruptured aneurysm of sinus of valsalva
Murmurs which change in character or intensity over
time:
Carey coomb’s murmur
Infective endocarditis
Atrial thrombus
Atrial myxoma
10
What is Gallaveredin phenomenon?
Gallaveredin phenomenon is a clinical sign that can
be seen in aortic stenosis.
Noisy, harsh component of the murmur is
heard at the upper right sternal border with
radiation to the neck
Musical component is heard at the apex and
can be differentiated from mitral
regurgitation as it doesn’t have radiation to
the axilla.
Abscess
Pericardial effusion
Ejection fraction (left ventricular ejection
fraction >55% is considered normal)
13. Cardiac MRI
14. Pericardial fluid analysis
15. Cardiac catheterization: especially for evaluation of
coronary arteries (valve replacement surgery)
Additional Information
Beck’s triad for cardiac tamponade (3Ds):

Investigation Modalities Distant heart sound

Decreased blood pressure
1. CBC: anemia, infection, inflammation (acute phase Distended neck vein
reactant - elevated platelet)
Loud S1 Increased cardiac
2. Electrolytes: K+, Na+, Ca2+, phosphate
output (pregnancy,
3. Cardiac enzyme (troponin, CK-MB): elevated in
anemia, tachycardia)
myocardial infarction and acute pericarditis Large stroke volume
4. Rheumatoid test, ANA, immunoglobulin complex: Mitral stenosis
autoimmune conditions (results in MS) Short PR interval
5. ESR/CRP: elevated in infective endocarditis, TB Atrial myxoma
6. Urinalysis: proteinuria Quiet/Soft S1 Low cardiac output
7. Liver function test, renal function test Poor left ventricular
8. Thyroid function test function
9. Biomarkers (BNP in failing heart) Long PR interval (first
10. Chest x-ray degree block)
Cardiac enlargement (>50% cardio-thoracic Rheumatic mitral
ratio) regurgitation
Pulmonary lesions Calcific mitral stenosis
Bat wing’s sign (cephalization of pulmonary Loud S2 Systemic hypertension
vessels) suggests cardio-pulmonary edema Pulmonary
hypertension
Cardiomegaly Normal heart size Quite S2 Low cardiac output
(CTR>50%) (CTR<50%) Calcific aortic stenosis
Regurgitant lesion Stenotic lesion Aortic regurgitation
Dilated cardiomyopathy Pulmonary hypertension
Pericardial effusion Cardiomyopathy
Par cardiac mass Hypertrophic
Pregnancy/ascites Restrictive
Obesity Myocardial infarction
Ischemic heart disease (new and acute)
11. ECG: identifies arrhythmia, conduction disturbance,
myocardial ischemia, QT prolongation syndrome
and metabolic syndrome (hyperkalemia).
12. Echo cardiography:
Size of the chambers
Ventricular wall thickness
Regional wall motion abnormality: indicates
myocardial infarction
Valvular lesions
Vegetation (infective endocarditis)

11
 Examination of the Abdomen
Compiled by: Veronica Zinabu

The abdomen houses some of the most important structures in the human body including the liver and the kidney.
Other important structures such as the stomach, small intestine, large intestine, spleen, lymph nodes as well as large
arteries and veins.

Abdominal examination is clearly not the most difficult physical examination to do, explaining why medical students
wish to encounter it during exams. But, as many senior physicians repeatedly say, it is the one examination that is very
tricky for the students. This is because, the likelihood of missing steps is increased and even what may be considered
trivial may matter a lot. For example, if the patient reported any site of pain, you should be able to distract the patient
by talking about something else while you palpate the area, and this may be considered as an important skill. The
abdominal examination, similar to the rest, should be done on the right side of the patient (unless the examiner is left
handed) and the inspection part should be done from the foot of the bed. Ideally, abdominal examination should be
done after emptying the bladder and per-rectal examination should also be done as the final step. These may not be
possible in the exam setting, but you can talk about it verbally.

Firstly, you need to know in what position the patient should be during the examination. The patient should be in the
supine position, with a pillow under the head and perhaps another pillow under the knees, to maintain comfort. The
arms should be placed on the sides. This is because, if the hands are above the patient’s head, the abdominal wall
stretches and tightens, making palpation difficult. Then you should expose the abdomen, from the xiphisternum to the
symphysis pubis.

Physical examination The first step in the examination is inspection and

should be done at the foot of the bed, looking at the
The abdominal examination can be summarized with abdomen from the front.
the next table with the orders in the bracket.
Symmetry: the normal abdomen is symmetrical and
Patient should be supine with pillow underneath the
asymmetric abdomen is likely due to a bulge from an
head and the hands on the side. He/she should be enlarged organ or a large tumor. A central bulge is most
exposed from xiphisternum up to the symphisis. likely due to an enlarged uterus, ovary or bladder.
Inspection (1) Palpation (3)
Symmetry Tenderness (deep Shape (contour, fullness, distention, scaphoid/sunken)
Shape and contour and superficial) Generalized fullness: obesity, pregnancy,
Umbilicus Mass (deep and intestinal obstruction (feces, flatus), ascites,
Skin superficial) enlarged organ (hepatomegaly, splenomegaly,
Abdominal wall Bimanual palpation of abdominal aorta aneurysm, or bladder
movement the kidneys distention), malignancies, abscess or cysts.
Hernias Liver palpation It can be remembered with the 6F’s: fat, fetus,
Visible vessels Spleen palpation feces, flatus, fluid and fatal growth.
Auscultation (2) Percussion (4) Localized distention:
Bowel sounds Tympanicity Symmetrical and around the umbilicus small
Bruits Direct and shifting bowel obstruction
Venous hums dullness Asymmetrical and gross enlargement of the
Friction rubs Fluid thrill liver, spleen or ovary
Total vertical liver Palpable enlargement of the lower abdomen
span stands for chronic urinary retention
Splenic percussion Scaphoid abdomen: starvation/malignancy

12
The umbilicus is normally centrally located, slightly
retracted and inverted
Everted/flat umbilicus: ascites, hernia
Upward displaced umbilicus: pregnancy, ovarian
cyst
Skin markings
Smooth and shiny: marked abdominal distention
White or pink wrinkled linear marks (striae
atrophica or gravidarum): pregnancy, ascites,
wasting diseases, severe dieting
Wide purple striae: Cushing syndrome,
excessive steroid treatment
Scars: surgical or not
Pigmentations: linea nigra during pregnancy
Prominent superficial veins
The 3 possible prominent superficial veins
1. Thin veins over the costal margin: not important
2. Occlusion of the inferior vena cava: the veins can
be seen on both the abdomen and the chest. If
the veins are prominent, you can check the
direction of flow by occluding a vein, emptying
it by massage and then looking for the
direction of refill. In this case the flow will be
upward (the veins that are dilated represent
anastomotic channels between the superficial
epigastric and circumflex iliac veins below, and
the lateral thoracic veins above, conveying the
diverted blood from the long saphenous vein to
the axillary vein, the direction of flow is therefore
upwards).
3. Venous anastomosis in portal hypertension can
give distended vessels around the umbilicus
(caput medusa). These distended veins
represent the opening up of anastomoses
between portal and systemic veins and occur in
other sites (esophageal and rectal varices).
Signs of portal hypertension in the abdomen are 3:
Caput medusa (uncommon)
Splenomegaly
Ascites
Abdominal wall movement involves movement during
respiration in a normal condition (rise of the abdomen
during inspiration and fall with expiration). Other
movements include:
Silent abdomen (markedly decreased or absent
movement): generalized peritonitis
Visible pulsation (abdominal aorta): frequent
finding in thin, nervous patients
Visible peristalsis of stomach and small intestine
The 3 causes of visible peristalsis
1. Obstruction of the pylorus: is due to fibrosis of a
long standing duodenal ulcer or by carcinoma of
the pyloric antrum. In pyloric obstruction, a
diffuse swelling may be seen in the left upper
abdomen but, where obstruction is longstanding
with severe gastric distension, this swelling may
occupy the left mid and lower quadrants. Such a
stomach may contain a large amount of fluid
and, on shaking the abdomen, a splashing noise
is usually heard (’succussion splash’). This splash
is frequently heard in healthy patients for up to
3 hours after a meal, so enquire when the patient
last ate or drank
2. Obstruction of distal small bowel
3. Normal finding in very thin, elderly patient with
lux abdominal muscles or large wide necked
incisional hernia seen through abdominal scar
Hernias: ask the patient to cough and look for incisional,
epigastric, umblical, femoral and inguinal bulging.
Inspection of a normal abdomen
Abdomen is full/flat, symmetrical, moving equally
with respiration. Umbilicus is central and inverted.
There is no scar, striae, pigmentation, prominent
veins, pulsations or peristalsis. Hernia sites are free.
The next step is auscultation and it should precede
palpation and percussion as this two affect the findings
on auscultation.
Bowel sounds: are widely transmitted through the
abdomen, as a result, listening by gently applying the
diaphragm of the stethoscope in one spot, such as the
right lower quadrant is usually sufficient. Normal
sounds consist of clicks and gurgles, occurring at an
estimated frequency of 5 to 34 per minute.
No bowel sound: paralytic ileus, peritonitis
Exaggerated bowel sound: diarrhea, intestinal
obstruction
Exaggerated bowel sound is heard in simple acute
mechanical obstruction of the intestine but if
obstruction progresses leading to bowel necrosis,
peristalsis ceases and sounds lessen in volume as well
as frequency.
13
Bruit: arterial bruits indicate turbulent flow in the
underlying vessels, due to stenosis, aneurysm or
malignant circulation.
Listen for bruits by light application of the stethoscope
above and to the left of the umbilicus (aorta), the iliac
fossae (iliac arteries), epigastrium (coeliac or superior
mesenteric arteries), laterally in the midabdomen (renal
arteries) or over the liver (increased blood flow in liver
seen classically primary liver cancer).
Friction rubs: are seen in cases of hepatoma, gonococcal
infection around the liver, splenic infarction, and
pancreatic carcinoma.
Palpation is the third step and involves superficial and
deep palpations.
Before touching the patient, always ask the patient if
there is an area of pain on the abdomen and make sure
to reassure the patient to relax, and then warm your
hands by rubbing them, don’t blow on them.
Start palpating the abdomen from an area where there
is no tenderness and continue to palpate anti-clockwise.
If there is no area of tenderness, start from the left
lower quadrant and move anti-clockwise.
Correct method of palpation: The hand is held flat &
relaxed & ‘moulded’ to the abdominal wall.
Incorrect method of palpation: The hand is held rigid
and mostly not in contact with the abdominal wall.
Correct palpation
Incorrect palpation
Correct deep
palpation in
obese, muscular
or poorly relaxed
patient
All the organs in the upper abdomen (liver, spleen,
kidneys, stomach, pancreas, gallbladder) move
downward with inspiration (with the spleen moving
more downwards and medially). Thus, asking the
patient to take a deep breath while examining makes
detection of these organs easier, since something that
is moving is easier to detect than something stationary.
However, to avoid confusing one’s sensation, when the
patient breathes in, the examining hand should be still
so that the organ in question ‘comes onto the examining
hand’, or ‘slips by’ underneath it.
Putting the left hand on top of the right allows increased
pressure to be exerted, such as with an obese or very
muscular patient.
A small proportion of patients find it impossible to relax
their abdominal muscles when being examined. In such
cases, it may help to ask them to breathe deeply, to
bend their knees up or to distract their attention in
other ways.
Superficial palpation intends to identify:
Tenderness, muscular resistance and superficial
masses
If resistance is present, try to distinguish the
voluntary guarding from involuntary muscular
spasm
Involuntary rigidity or muscular spasm is suggestive of
peritoneal inflammation.
14
In deep palpation we look for before it becomes palpable, and then is felt beneath the
left subcostal margin.
Abdominal masses, organomegally

Note the Site, Size, shape, surface, edge, consistency,

mobility and attachments, bimanual palpability and
pulsatile nature of any palpable mass.

If the swelling is in the upper abdomen, try to determine

if it is possible to ‘get above it’; that is, to feel the upper
border of the swelling as it disappears above the costal
margin, and similarly, if it is in the lower abdomen,
whether one can ‘get below it’. If one cannot ‘get
above’ an upper abdominal swelling, a hepatic, splenic,
renal or gastric origin should be suspected. If one
cannot ‘get below’ a lower abdominal mass, the
swelling probably arises in the bladder, uterus, ovary or
occasionally the upper rectum.
The pathological nature of a mass is suggested by a
number of features. A swelling that is hard, irregular in
outline and nodular is likely to be malignant, while
a regular, round, smooth, tense swelling is likely to
be cystic. A solid, ill-defined and tender mass suggests
an inflammatory lesion as in Crohn’s disease of the
ileocaecal region.
If the swelling is fixed, it could be:
A retroperitoneal origin
Part of an advanced tumor with extensive
spread to the anterior or posterior abdominal
wall or organs
A swelling resulting from severe chronic
inflammation involving other organs such as
tuberculous ileocaecal mass.
Palpation of the spleen: start well out to the left
Normally the urinary bladder is not palpable. When it is
full and the patient cannot empty it (retention of urine),
a smooth firm regular oval-shaped swelling will be
palpated in the suprapubic region and its dome (upper
border) may reach as far as the umbilicus.
Carefully note whether a swelling is pulsatile, and
decide if any pulsation comes from the mass or is
transmitted through it.
Remember: Where considerable splenomegaly is
present, its typical characteristics include a firm swelling
appearing beneath the left subcostal margin in the left
upper quadrant of the abdomen, which is dull to
percussion, moves downwards on inspiration, is not
bimanually palpable, whose upper border cannot be felt
(i.e. one cannot ‘get above it’) and in which a notch can
often, though not invariably, be felt in the lower medial
border. The last three features distinguish the enlarged
spleen from an enlarged kidney; in addition, there is
usually a band of colonic resonance anterior to an
enlarged kidney.

Bimanually palpable swellings in the lumbar region are

usually renal in origin. Kidney is not usually palpable
unless either low in position or enlarged. Its lower pole,
when palpable, is felt as a rounded firm swelling
between both right and left hands (i.e. bimanually
palpable) and it can be pushed from one hand to the
other, in an action which is called ‘ballotting’.

Palpation of the liver: either method can be

used, but the upper one is preferable.

Bimanual palpation of the left kidney

Like the left kidney, the spleen is not normally palpable.

It has to be enlarged to two or three times its usual size

15
The next step is percussion. The percussion note of a
normal abdomen is tympanic, with the exception of the
liver area, which is dull. A normal spleen is not large
enough to give a dull note.
Measure the total liver span as follows:
Starting at a level below the umbilicus in the right lower
quadrant (in an area of tympany, not dullness), percuss
upward toward the liver. Identify the lower border of
dullness in the midclavicular line. Next, identify the
upper border of liver dullness in the midclavicular line.
Starting at the nipple line, lightly percuss from lung
resonance down toward liver dullness. Gently displace
a woman’s breast as necessary to be sure that you start
in a resonant area. Now measure in centimeters the
distance between your two points: the vertical span of
liver dullness.
Remember that liver dullness may be displaced
downward by the low diaphragm of chronic obstructive
pulmonary disease. The span, however, remains
normal.
You can check for fluid collection in the abdomen
through two steps:
Shifting dullness: sensitive
Fluid thrill: positive only when the fluid is large
in volume, thus not reliable
Eliciting fluid thrill
When a spleen enlarges, it expands anteriorly,
downward, and medially, often replacing the tympany
of the stomach and the colon with the dullness of a solid
organ. People used this fact to come up with percussion
maneuvers to identify splenomegaly.
1. Traube’s semilunar space
Borders: superiorly (left 6th rib), laterally (left
midaxillary line/left anterior axillary line), inferiorly
(left costal margin)
Patient’s position: supine with left arm slightly
abducted
Percussion: from medial to lateral
Interpretation: resonance is the normal finding and
dullness shows splenomegaly (Pleural effusion or
mass in stomach may cause dullness in Traube’s
space)
2. Castell’s method
Patient’s position: supine
Percussion: in the lowest intercostal space in the
anterior axillary line (8th or 9th)
Interpretation: resonant on expiration or full
inspiration is the normal finding and dullness on full
inspiration shows splenomegaly
3. Nixon’s method
Patient’s position: right lateral decubitus (spleen
comes to lie above colon and stomach)
Percuss: midway along the left costal margin and
proceed in a line perpendicular to left costal margin
Interpretation: upper limit of dullness >8cm above
costal margin shows splenomegally
Important findings
Although there may be several findings on abdominal
examination, the most widely asked are:
Ascites
Splenomegaly
Hepatomegaly
Differential diagnosis for ascites include:
Cirrhosis (84 % of ascites)
10-15% of ascites is accounted by cardiac ascites,
peritoneal carcinomatosis and mixed ascites
16
 Other causes: massive hepatic metastasis, Gross appearance of fluid
infection (Chlamydia, TB peritonitis),
Turbid: infection, tumor cells
pancreatitis, nephrotic syndrome
White/milky fluid: with a triglyceride > 200mg/dl
Rare causes: hypothyroidism, familial
(often>1000mg/dl) is chylous ascites (trauma,
Mediterranean fever
cirrhosis, tumor, TB, Congenital anomalies)
Ascites in the absence of cirrhosis: Dark brown: high bilirubin indicating a biliary
tract perforation.
Peritoneal carcinomatosis, peritoneal infection Black: pancreatic necrosis or metastatic
(TB), or pancreatic disease. melanoma
Tumor cells lining the peritoneum produce a
protein rich fluid that contribute to the Investigation from the fluid: albumin, total protein
development of ascites. levels, cell count and differential, gram’s stain, culture
Tubercles deposited on the peritoneum exude a
Serum-ascites albumin gradient (SAAG): differentiates
proteinaceous fluid.
ascites of portal hypertension from non-portal
Pancreatic ascites results from leakage of
hypertension ascites. It is important to know that SAAG
pancreatic enzyme into the peritoneum.
doesn’t change with diuresis.
Peritoneal carcinomatosis:
Primary peritoneal malignancy: mesothelioma or
sarcoma
Abdominal malignancies: gastric or colon
adenocarcinoma
Metastatic disease: breast or lung Carcinoma,
melanoma

Ascites of cirrhosis is the result of portal HTN as well as

renal salt and water retention.

Ohm’s law suggests that pressure is a product of

resistance and flow.

Mechanisms for increased hepatic resistance

Hepatic fibrosis (cirrhosis) – disrupts normal

architecture of hepatic sinusoids and impedes
normal blood flow through liver.
Activation of hepatic stellate cells, which mediate
fibrogenesis, leads to smooth muscle contraction
and fibrosis.
Decreased intrahepatic endothelial nitric oxide
synthetase (eNOS) production leads to decreased
nitric oxide production increased intrahepatic
Other investigations for ascites
vasoconstriction.
Secondary peritonitis
In response, there will be increment in systemic level of
nitric oxide leading to splanchnic arterial vasodilation Ascitic glucose < 50mg/dl
pooling of blood and decrease in effective circulating Ascitic LDH > serum LDH
volume, which is perceived by kidney as hypovolemia Multiple pathogens on ascitic fluid culture.
RAAS activation renal sodium and water retention
Pancreatic ascites (ascitic amylase > 1000 mg/dl)
Evaluation of ascites
Cytology (at least 50ml)
The left lower quadrant is the preferable site for
paracentesis because of its larger depth (no organ Peritoneal carcinomatosis
damage) and thinner abdominal wall.

17
 Tuberculous peritonitis: if there is ascitic fluid
lymphocytosis in patients without cirrhosis, and
ascitic ADA has sensitivity >90% (cut off value
30-45 U/L)
Splenomegaly: can be caused by different pathology.
Causes of splenomegaly (in cm below the left lower
costal margin along the line of growth)

Uncertain cause: laparotomy, laparoscopy with Massive Chronic malaria

peritoneal biopsy for histology and culture remains the Visceral leishmaniasis (kalazar)
(>8 cm)
gold standard. Chronic myeloid leukemia (CML)
Myelofibrosis
Complications of ascites Primary lymphoma of the spleen
Spontaneous bacterial peritonitis (SBP) Portal hypertension (rarely)
Patients note increase in abdominal girth, Moderate Causes of massive splenomegaly
tenderness (only in 40%) Portal hypertension
Poly-morpho-nuclear > 250/L in ascitic fluid (4-8 cm)
Leukemia, lymphoma
Presence of multiple pathogens without Thallasemia
elevated PMN count suggests bowel perforation Gaucher’s disease
from the paracentesis needle.
Treatment: IV cefotaxime for 5 days Small All causes listed above
Prophylaxis: Patients with history of SBP, ascitic Polycythemia
(2-4 cm)
fluid total protein < 1 g/dl, and active GI bleeding Hemolytic anemia
should be given Norfloxacin PO daily Hepatitis
Hepatic hydrothorax Infective endocarditis
Infectious mononucleosis (CMV)
Management of ascites SLE
Cirrhotic ascites Rheumatoid arthritis
Polyarteritis nodusa
Restrict sodium intake to 2g/d
Oral diuretics: spironolactone + furosemide Causes of hepatomegaly
Substitue amiloride (5-40mg/d) if side effects of Causes of a true hepatomegaly based on etiology
spironolactone occur
If no response with sodium restriction and Bacterial Parasitic
maximal daily doses of spironolactone (400mg)
Liver abscess Malaria
and furosemide (160mg), it is called refractory.
Typhoid Kalazar
Refractory cirrhotic ascites Brucellosis of liver Schistosomiasis
Syphilis of liver Hydatid cyst
Add midodrine or clonidine to diuretic therapy
(vasoconstrictors to counteract splanchnic Viral Early cirrhosis as in
vasodilation) alcoholic liver disease
Hepatitis
Repeated large volume paracentesis (LVP): an IV
Infectious
albumin infusion of 6-8 g should be given for
mononucleosis
every 1 liter of ascitic fluid removed.
TIPS: reduces re accumulation, but increases Congestive Neoplastic
frequency of hepatic encephalopathy
CHF Hepatocellular
Malignant ascites (doesn’t respond to Na restriction and Constrictive carcinoma
diuretics) pericarditis Cholangiocarcinoma
Metastasis
Serial large volume paracentesis (LVP), Budd-chiari syndrome
Leukemia/lymphoma
transcutaneous drainage catheter placemenet
Myeloproliferative
or rarely peritoneo-venous shunt with IVC.
disorders
TB peritonitis: standard anti-TB regimen

18
Investigations 4. CT/MRI

Other than the peritoneal fluid analysis you can also

mention other investigations based on your finding.

Lab investigations

1. CBC
Anemia
Thrombocytopenia
2. Coagulation profile (PT, PTT, INR)
3. LFT, RFT

Endoscopy (upper GI, lower GI)

Imaging

1. Plain abdominal X-ray

2. Ultrasound (biliary tract, ascites, mass)
3. CT/MRI

19
 Lower Motor Examination
Compiled by: Metasebia Zewdu

Normal motor function is a result of integrated activity between the cerebral cortex, internal capsule, basal ganglia,
cerebellum, spinal cord, peripheral nerves & muscles. Any abnormality in this pathway can lead to paresis, which is a
reduction in power exerted by muscles. Although there is no uniform consent on the distinction between paresis &
plegia, what most clinicians agree on is that paresis is a mild to moderate weakness of the muscles (with a power of
1,2,3,4), while plegia is a complete weakness of the muscles (0 power).

Based on the limbs that are involved by the weakness we can classify it as hemiparesis (involving one half of the body),
paraparesis (involving both the lower limbs) and quadriparesis (involving all the four limbs). Some examiner prefer if
you use the term monoparesis, if there is a hemiparesis and you are doing only the lower motor examination. In this
section, the steps of lower motor exams and the interpretations will be discussed shortly.

Lower motor examination
Like the other physical examination, you should start by
inspection of the legs and feet.
Position of feet/leg: deviation of the feet implies
weakness. If the feet are rotated outwards we can
expect a spastic paralysis (upper motor neuron) and
if the rotation is to the midline, a flaccid paralysis
(lower motor neuron).
Muscle bulk: you must first see if there is a visible
discrepancy of the muscle bulk in corresponding
areas of the two limbs and then measure with a tape
meter 10cm below and 20cm above the tibial
tuberosity, then compare. A reduced muscle bulk is
suggestive of lower motor neuron lesions although
it can happen in a long standing upper motor neuron
lesion due to disuse atrophy. If there is a difference
in the measurement with swelling and tenderness
you should suspect DVT, as limb weakness is a very
important risk factor for its development.
Fasciculation: are twitching of the muscles visible
through the skin suggesting lower motor neuron
lesions. You should first see if there is a spontaneous
fasciculation and then try to induce it by tapping on
areas of muscle bulk with your hammer.
You can also inspect for any skin lesions including
scars and leg deformities.
After finishing the inspection, you then should proceed
to assessing the tone, power and reflexes.
The tone is the resistance to passive movement of the
limbs. You should check the tone by moving the feet,
the leg and the thigh. A decreased tone (hypotonic) is a
manifestation of lower motor lesion and a tone
increment (hypertonic) suggests an upper motor lesion.
You report this as hypertonic, hypotonic or normotonic.
You can assess the power by seeing the movement of
the leg independent of gravity, against gravity, and with
the application of some resistance. You grade power
out of 5 as:
0 (no movement)
1 (flickering of feet)
2 (active movement with gravity eliminated)
3 (active movement against gravity)
4 (active movement against some resistance)
5 (active movement against full resistance)
It is often better to start by asking the patient to raise
the legs against gravity and assess the others based on
the outcome. If he/she couldn’t raise it go down in to
assessing side to side movement (no gravity) and if
he/she could raise the legs try assessing movement with
some resistance.
Another way of assessing the power is checking for each
muscle group.
Dorsiflexion & plantarflexion: elevate/press down
the feet & toes against resistance
Extension of knee: bend the knee & try to straighten
against resistance

20
 Flexors of knee: raise the leg from the bed & ask the
patient to bend their knee
Extension of hip: raise the leg with the knee
extended & ask the patient to push down against
resistance
Flexors of hip: extend the knee & ask the patient to
raise the leg against resistance
Adductor of thigh: abduct the leg & ask the patient
to bring the legs to the midline against resistance
Abductor of thigh: put the legs together in the
midline & ask the patient to separate them against
reistance
Rotators of thigh: extend the knee & ask the patient
to rotate internally & externally againstt resistance
The deep reflexes are assessed by stroking the tendons
with your hammer and grading as follows.
0 no response
+ depressed (plus 1)
++ normal (plus 2)
+++ exaggerated (plus 3)
++++ exaggerated & clonus (plus 4)
An exaggerated reflex and a clonus is suggestive of
upper motor neuron lesion while a depressed reflex is a
sign of a lower motor involvement. Although a reflex of
+3 is considered abnormal, it may be seen in the knee
reflex of normal people as well. In lower motor
examination you should check for ankle and knee
reflexes and clonus.
Superficial reflexes should also be done, in lower motor
exam you especially can’t omit plantar reflex.
Abdominal reflex can be absent in upper motor
neuron lesions
Cremasteric reflex: done only on male patients,
when you lightly trace the medial aspect of the
thigh, the scrotum moves upward.
Plantar reflex is normally down going. But it
becomes upgoing (dorsiflexion of the great toe &
fanning of the other toes) in upper motor neuron
lesions. It is reported as down going, up going or
equivocal.
Coordination test and gait are not usually included in
exams, but could be helpful at times.
The presence of sensory level is suggestive of spinal
cord lesion and should be checked. The sensory
parameters are pain, temperature, vibration and
position senses. The lesion is usually 2 levels lower than
the spinal cord level as they cross higher up (for
example, if we get a sensory level at C2 then the lesion
is at C4).
Dermatome Spinal cord level
Clavicle C4
Tip of small finger C8
Nipple T4
Umblicus T10
Inguinal L1
Knee L4,5
Ankle S1
Cortical sensory tests such as two-point discrimination,
stereognosis and graphstesia will be affected in cortical
lesions.
Usually the lower motor examination ends with the
superficial reflex (plantar reflex in particular).
Paraparesis
A number of parameters we obtain from the history and
physical examination actually help us in narrowing
down our differentials and in localizing where the lesion
might be. For example, if we see the onset of weakness,
acute onset weakness speaks for vascular causes, acute
hydrocephalus, infections like transverse myelitis and
trauma. Vascular causes can be sagital sinus vein
thrombosis, parasagital cortical vein thrombosis,
anterior spinal artery ischemia or hemmorhage.
Subacute to chronic onset suggests compressive
myelopathy secondary to TB spondylitis, primary spinal
cord tumors or metastases, degenerative disorders of
the spinal cord
The types of muscle groups affected can also help us
differentiate the possible cause. For example,
myopathies tend to affect the proximal muscle groups,
so patients are going to have difficulties with climbing
stairs, arising from squatting position, combing their
hair or picking high-sitting objects. Neuropathies affect
the distal muscle more, meaning the patient is going to
be complaining of problems with their fine motor skills.
21
This table shows possible differentials for paraparesis
based on the duration of the weakness.
Cerebral paraplegia can inturn be secondary to:
Acute (<2 weeks) Subacute (2-6 weeks) or
Cerebral diplegia
chronic (>6 weeks)
Superior sagittal sinus thrombosis
Epidural abscess Chronic spinal cord Parasagittal cortical venous thrombosis
Spinal cord ischemia compression Parasagittal meningioma
Transverse myelitis Potts disease (AKA TB Hydrocephalus
Disc herination spondylitis) Thrombosis of unpaired anterior cerebral
GBS Multiple sclerosis
artery
Anterior cerebral Tumors
artery ischemia Subacute combined Gunshot injury of the paracentral lobule
Sagittal sinus degeneration
Spinal origin: the spinal lesions that can lead to
thrombosis Parasagittal
Cortical venous meningoma paraplegia are secondary to:
thrombosis Syringomyelia Cord compression
Acute hydrocephalus
Vascular: spinal cord infarction or hemorrhage
Tumor bleeding
Since paraparesis/plegia can be caused by both upper Infections: such as transverse myelitis and
neuro-syphilis
motor and lower motor lesions it is important to
differentiate the two. Systemic degeneration of tracts including:

Multiple sclerosis
Upper motor Lower motor
Muscle bulk unaffected Reduced muscle bulk Motor neuron disease
Hypertonic Hypotonic
Syringomyelia
Muscle group affected Individual muscle affected
Exaggerated deep Reduced/absent deep Subacute degeneration of the spinal cord
tendon reflex, there tendon reflexes, clonus is Motor neuron disease is unique in that it can display the
may be clonus absent signs of both upper motor and lower motor neuron
Abdominal reflex lost Intact abdominal reflex lesions at the same time.
Extensor (up going) Flexor (down going)
Spinal cord compression is of different types and can
plantar reflex plantar reflex
manifest with:
Fasciculation absent Fasciculation present
Causes of paraplegia Pain that could be localized over the spine or
over the root distribution (radicular pain). It
Cerebral origin: the lower limbs and the micturation
tends to get worse by coughing, sneezing or
center are represented in the paracentral lobule
straining
(around the upper one inch of the cerbral cortex) and as
Sensory changes: this includes parasthesia,
a result lesions of this area can give us paraparesis with
numbness to pain & T° changes usually
bladder disturbance (urine retention, urgency or
spreading proximally to a level on the trunk
incontinence).
Motor weakness (paraparesis)
This makes it similar to spinal cord lesions which can Bladder/Bowel incontinence: urgency &
also give us paraparesis with bladder dysfunction. As a hesitancy eventually leading to retention and
result presence of certain conditions should tip us some later on incontinence
information to localize the lesion to the cerebral cortex.
Based on the origin of the lesion, spinal compression
These tips are:
can be divided in to 3 as:
Aphasia
Extradural: origin from vertebra
Seizure Intradural: origin from meninges
Intramedullary: origin from the spinal cord
Apraxia
We get lower motor neuron type lesion at the level of
Cortical sensory loss (loss of graphstetsia,
compression as anterior horn cells are affected but we
sterognosis)

22
get upper motor neuron type of lesion below the Spinal cord level Vertebral level
compression because of corticospinal tracts affection. Upper cervical Same as cord segment
Lower cervical 1 level higher
Upper thoracic 2 levels higher
Lower thoracic 2-3 levels higher
Lumbar T10,11,12
Sacral T12-L1
Coccygeal L1
A compressive myelopathy can be differentiated from
the other causes of spinal paraparesis by the differences
presented on the following table.

Compressive Non-compressive
Vertebral tenderness or Absent
deformity present
Prominent root pain Absent
Intramedullary spinal cord compressions are mostly Usually asymmetrical Usually symmetrical
secondary to an intramedullary tumor. But the Gradual onset May be acute
extramedullary compressions have many differentials.
Flexor spasm present Absent
Extradural compression Intradural compression Other cause of spinal paraparesis is the cauda equina
Potts disease Epidural abscess syndrome. Difference with conus medullaris

Metastases Tumors (meningoma, Conus medullaris Cauda equina

lymphoma, metastases) Symmetrical involvement Asymmetrical
Multiple myeloma No root pain Severe low back pain
Most metastasis are No limb weakness Asymmetrical weakness
Intervertebral disc
from lung, breast, renal
prolapse Absent bulbocavernous Variable areflexia which
cell carcinoma,
(S2-S4) and anal (S4-S5) is dependent on the roots
Dislocation of vertebrae lymphoma and
reflexes involved
2° to fracture melanoma
Bilateral saddle Asymmetric sensory loss
Cervical spondylosis anesthesia
Bladder/bowel common Relatively spared
You can tell intramedullary and extramedullary lesions Extensor plantar (but not Normal or not elicitable
apart by the differences in the next table: always)
Extramedullary Intramedullary Flaccid paralysis is what we commonly call lower motor
neuron lesion and is due to lesions of the anterior horn
Root pain (radicular pain) Root pain are rare
cells, nerve roots, peripheral nerves and muscles. They
are common
are presented on the following table as follows.
Early corticospinal signs Late corticospinal signs
Brown-sequard syndrome Dissociated sensory loss Site of involvement causes
if lateral cord compression Anterior horn cell Poliomyelitis
Lower motor neuron signs Lower motor neuron Nerve root Radiculitis, polyradiculo-
to localized segment signs to several segment neuropathy, tabes dorsalis,
No sacral sparing Sacral sparing present cauda equina
Late bladder/bowel Early bladder/bowel Peripheral nerves GBS, peripheral neuropathy
Extramedullary stands for both the intradural and Myoneural junction Myasthenia gravis,
extradural lesions. myasthenia-myopathic
syndrome (Lambert-Eaton
If a patient reports a band of hyperalgesia on the trunk
syndrome), periodic paralysis
can help us in localising the level of spinal cord affected.
(hypo or hyperkalaemic)
Localization of spinal segment level can help identify the
Muscles Myopathy
vertebral level as follows.

23

Causes of pure motor paraplegia:
Cerebral causes of paraplegia
Spinal cord lesions such as:
Heriditary spastic paraplegia
Lathyrism
ALS
Acute demyelinating polyneuropathy
Myopathy
Hemiparesis
Hemiparesis results from an UMNL above the mid
cerivcal cord (most are above the foramen magnum).
Presence of other neurologic deficits will help us localize
the lesion. For example, presence of language disorders,
cortical sensory disturbance, cognitive abnormalities,
apraxia, seizure and disorders of visual-spatial
integration indicate cortical lesions while homonymous
visual field defects indicate a cortical or subcortical
hemispheric lesion.
A pure motor hemiparesis of face, arm and leg is mostly
due to lesions in the internal capsule or brainstem.
In acute hemiparesis, we usually evaluate the patient
with CT scan and lab tests, and do MRI of the brain or
spine if the CT doesn’t show any abnormality.
In subacute hemiparesis, the first investigation should
be brain MRI and if it is normal do MRI of the spine.
Quadriparesis
Weakness of all 4 limbs may occur secondary to
disorders of the CNS (quadriparesis) or motor unit
(generalized weakness).
Weakness from CNS disorders is usually associated
with:
Change in consciousness or cognition
Hypertonia
Exagerrated reflexes
Altered sensation
Most neuromuscular causes are associated with:
Normal mental function
Hypotonia
Diminished reflex

The abscence of cranial nerve deficits indicate that the Causes of quadriplegia could be:
lesion is in the cervical spinal cord, especially if it is
Cerebral palsy
associated with ipsilateral loss of proprioception (as this
Bilateral brainstem lesion
fibers cross high up in the medulla) and contralateral High cervical cord compression, e.g.
loss of pain and temperature. craniovertebral anomaly (atlantoaxial
Hemiparesis can be divided in to three based on the dislocation), high spinal cord injury (C1-C4)
duration of the weakness as acute (<2 weeks), subacute lesion, etc.
(2-6 weeks) and chronic (>6 weeks). The possible causes Multiple sclerosis
also differ based on the duration. Motor neuron disease
Acute anterior poliomyelitis
Acute hemiparesis Stroke, bleeding brain Guillain-Barre syndrome
tumor, trauma, abscess, Peripheral neuropathy
multiple sclerosis and Myopathy or polymyositis
sarcoidosis Periodic paralysis (transient quadriplegia)

Subacute hemiparesis subdural hematoma,
abscess, fungal
granuloma, meningitis,
parasitic infection,
primary tumor or
metastases, multiple
sclerosis and sarcoidosis
Chronic hemiparesis Neoplasms, vascular
malformations, chronic
subdural hematoma,
degenerative diseases
Acute quadriparesis may be secondary to upper motor
neuron disorders (hypotension, brainstem or spinal
cord ischemia, trauma, metabolic abnormalities) or
muscle disorders (electrolyte disturbance, inborn errors
of muscle energy metabolism, toxins and periodic
paralysis). It may also be caused by GBS.
Causes of episodic weakness:
Hyperthyroidism
Myasthenia Gravis
GBS

24
 Periodic paralysis (hypokalemic,
hyperkalemia, hypercalcemia,
hyponatremia, hypernatremia)
Conn’s syndrome also known as primary
hyper-aldosteronism
Botulinum poisoning
CNS disorders (transient ischemic attack of
the brain stem, Transient global cerebral
ischemia, Multiple sclerosis)

Investigation Modalities
1. AP and lateral X-ray of spine (features of TB,
herination of disc, secondary deposists, fracture and
dislocation of the vertebrae and cervical
spondylosis)
2. MRI: is the gold standard
3. Others (depending on the diagnosis):
CBC, ESR, peripheral smear
FNAC or lymphnode biposy
Chest x-ray: TB, lung cancer or
lymphoma
CSF examination
Abdominal ultrasound to look for mass,
ascites, hepato-spleno megally
Abdominal CT
Chest CT
PICT

25
 Examination of the Lymphatic System
Compiled by: Michael Yeshiwas

In certain literatures of physical diagnosis, you may find this topic as lympho-glandular system together with the breast,
thyroid, testicles and parotid glands. But, this would be a very long examination and not suited to exam purposes.
Instead, it is the lymphatic system that appears on exams.

The lymphatic or lymphoid system comprises the lymph, the lymphatic vessels, lymph nodes, the thymus and the
spleen. Its main functions includes:

removal of interstitial fluid from tissues

absorption and transport of fatty acids and fats as chyle from the digestive system
transport of white blood cells to and from the lymph nodes into the bones
transport of antigen-presenting cells such as dendritic cells, to the lymph nodes where an immune
response is stimulated

The diagnosis of a patient with lymph node enlargement is very challenging due to the various differential diagnosis of
the conditions. Another challenge may be the discrepancy on the size of the lymph nodes at different ages of
development (larger in adolescents) and the repeated enlargement of the inguinal and submandibular lymph nodes
following simple infections or recurrent trauma. The lymph node enlargement can be localized or generalized. It has
been a relatively rare possibility to encounter this case for a short exam. But, when it occurs to you it is a 100% and
getting ready wouldn’t be the worst idea.

Physical examination are shown in the next picture and need to be included
in your examination as well.
Lymph node examination is not as complex as the other
physical examinations and heavily relies on inspection
and palpation. A knowledge on the site of the lymph
nodes is vital and is displayed on the pictures.

Inspection is done when you find an area of lymph node

enlargement. Once you find the enlarged node, you
should see if the area is erythematous and if it is
draining pus (sinus tract).

When you palpate, it is better to palpate by using the

This picture shows areas of lymph nodes in the body:
fingers of your two hands to palpate similar nodes of the
supraclavicular, axillary, epitrochlear and inguinal nodes
two sides simultaneously. But, this works for some
should be palpated on the exam.
nodes of the head and neck only: posterior auricular,
The location of lymph nodes in the head and neck region preauricular, submandibular and supraclavicular nodes.

26
When you palpate the cervical nodes, you can increase Infectious (viral, bacterial, fungal, chlamydial,
the access by turning the head of the patient to the parasitic or rickettsial)
opposite side. It is also a good idea to check for thyroid
Immunologic diseases
gland enlargement after palpating the cervical nodes
(confirm the mass by palpation and ask the patient to Malignant diseases (hematologic or metastatic)
swallow and see the movement, if the mass moves it is
Lipid storage diseases
of thyroid origin).
Endocrine diseases
Make sure to check for the nodes symmetrically (don’t
proceed to another node group without checking the Other disorders
same node group of the opposite side). Once you find
Investigation modalities
all the enlarged nodes, you need to measure the size.
Based on the involved area you can report it as local, 1. Laboratory tests
regional or generalized lymphadenopathy. CBC and peripheral morphology
ESR
You should also report the following
PICT (HIV)
Characteristics of lymph nodes RPR/VDRL (syphilis)
ANA (SLE)
Location
Hetrophile antibody test
Size
LDH
Consistency: soft, firm, hard
2. Imaging studies
Fixation: mobile or immobile, matted or
Chest X-Ray
discrete
Ultrasonography & Doppler
Tenderness
Nuclear/Isotope scans
Temperature
CT-Scan
Malignant conditions tend to give hard and MRI
immobile lymph nodes. PET/SPECT

Infectious cases may have soft and tender nodes. Imaging modalities are used to define size and
distribution more precisely, distinguishing from similar
Tuberculosis may have matted nodes. structures, staging and guiding fine needle aspiration
Virchow nodes: are enlarged left supraclavicular nodes (FNA).
and are bad omens as they are associated with intra- 3. Lymph node biopsy
abdominal malignancies.
Inguinal nodes are not favorable for this study due to
Mechanisms of lymphadenopathy the low yield. Supraclavicular, cervical and axillary
nodes are all preferable. Open biopsy is preferable for a
Lymph node enlargement can be a result of one or more
single enlarged node. FNA and core needle biopsy are
of the following mechanisms:
other alternatives. The specimen can be studied with:
Benign proliferation of residential cells (HIV/RVI)
Pathology
Infiltration by inflammatory cells (can be due to
Immunochemistry/immunophenotype
infections or autoimmune conditions)
Genetic/molecular studies
In situ proliferation of Malignant lymphocytes as
4. Bone marrow aspiration/biopsy
in lymphomas
Infiltration of lymph nodes by metastatic
malignant cells (breast, colorectal, Lung cancer)
Infiltration of lymph nodes by metabolite-laden
macrophages (lipid storage diseases)

Through the above mechanisms, several pathologic

conditions can result in lymphadenopathy including:

27
 References
Hutchisons' Clinical Methods, 23rd Edition
Bates' Guide to Physical Examination, 11th Edition
Harissons' Principles of Internal Medicine, 19th Edition

Edited by:
Metasebia Zewdu
Michael Yeshiwas
Good Luck on your Exam!
Minale Menberu
Veronica Zinabu